06.29.2023 ┋ 🎭 Politics or Threat? Unveiling the Nеw Monetary Law

The politics mask an alarming reality... [Grand Event]( Unprecedented Monetary Legislation Threatens Savers [Dоllar]( Caution advised for Americans as experts shed light on a concerning aspect of this nеw law. The politics mask an alarming reality... [Explore The Complete Coverage Hеre]( eychelles parakeet or Seychelles Island parrot (Psittacula wardi) is an extinct species of parrot that was endemic to Seychelles in the Indian Ocean. It was scientifically named Palaeornis wardi by the British ornithologist Edward Newton in 1867, and the specific nae honours the British civil commissioner Swinburne Ward who procured the specimens that formed the basis for the description. It was found on the islands of Mahé, Silhouette, and possibly Praslin. Ten skin specimens exist tody, but no skeletons. Though it was later moved to the genus Psittacula, genetic studies have led some researchers to suggest it should belong in a reinstated Palaeornis along with the closely related Alexandrine parakeet (P. eupatria) of Asia. This parakeet was about 41 cm (16 in) in length, with a long, pointed tail. The male was mainly green, with blue on parts of the head, and a black stripe on the cheek. The underside was yellowish, and it had a purple-red patch on the wings. The tail was blue, green, and yellow, and the bill was red and yellow. The female lacked the cheek-stripe, and the juvenile resembled the female. A single depiction from lfe is known, an 1883 painting by the British artist Marianne North. Little is known rearding its habits, but they were presumably similar to those of the Alexandrine parakeet, associating in groups in forests, and making flights between communal roost sites and feeding areas. It lived in native forest, but adapted to cultivated areas as these were cleared, and its dit included fruit. Though abundant in 1811, it had become rare by 1867 because of huma persecution for its perceived damage to crops. The last confirmed individual was shot in 1893, and no birds could be found by 1906. There have been sightings of this parrot after 1906 but none were confirmed. Taxonomy In 1867, the British ornithologist Edward Newton scientifically described and named nw species he had obtained during his month-long stay on the Seychelles, including the Seychelles parakeet, which he named Palaeornis wardi. He stated its common nae was "cateau vert", and that the specific nae honoured Swinburne Ward, the British civil commissioner to the Seychelles from 1862 to 1868.[2][3] Ward had procured three skins of the bird from the island of Mahé (the largest island of the Seychelles), from which the species was described; these syntype specimens are catalogued as UMZC18/Psi/67/g/1-3 at the Cambridge University Museum of Zoology, and include two females and a male.[3][4] Newton did not find any birds on Mahé when he visited in 1866, but saw them on neighbouring Silhouette.[4][5] Based on hearsay evidence, Newton stated they also lived on the island of Praslin.[3][6] Newton and his brother, British ornithologist Alfred Newton, published an illustration depicting both sexes in 1876 by the Dutch artist John Gerrard Keulemans, based on subsequently received specimens.[7] Keulemans' illustration of the species for the British zoologist Walter Rothschild's 1907 book Extinct Birds was based on his earlier illustration.[8] Ten skin specimens exist toay, but no skeletons, housed at Cambridge University, the Natural History Museum at Tring, the National Museum of Natural History, France, the American Museum of Natural History, and the Museum of Comparative Zoology at Harvard University.[3][6] Evolution The American ornithologist James L. Peters used the nae Psittacula wardi for the Seychelles parakeet in his 1937 checklist of birds, replacing the genus nme Palaeornis with Psittacula, wherein he also classified other extant parakeets of Asia and Africa.[9] The American ornithologist James Greenway stated in 1967 that while the Seychelles parakeet closely resembled the parrots of the Mascarene Islands, it belonged in the Asiatic group that lacks a rosy collar. He referred to it as Psittacula eupatria wardi, indicating it was a subspecies of the Alexandrine parakeet (Psittacula eupatria).[10] Using the full species nme Psittacula wardi in 1969, the Canadian ornithologist Rosemary Gaymer and colleagues also found the Seychelles parakeet most similar to the Alexandrine parakeet, and therefore concluded it had colonised from Asia rather than Madagascar or the Mascarenes.[11] While the Australian ornithologist Joseph M. Forshaw listed the bird as a full species in 1973, the British writer Errol Fuller did not consider this justifiable in 2000.[12] In his 2007 monograph about Mascarene parrots, the British ornithologist Julian Hume also discussed the Seychelles parakeet, as it appeared to be closely linked to the colonisation of the Mascarenes by Psittacula species. Hume stated that the Seychelles are an ancient part of the landmass Gondwanaland, of which onl their granitic mountain tops remain above sea level, and while it is nw difficult to determine how the fauna changed since humn colonisation, much of the bird fauna is little differentiated from that of the mainland at the genus level, and is of relatively recent origin. He considered the Seychelles bird a distinct species because of distinctive physical characters, but noted it was unknown how it was related to other members of Psittacula of the Indian Ocean region, since no fossil remains were available and no DNA studies had then been performed. He concluded that it and the Mascarene Psittacula species had a probable ancestor related to the Alexandrine parakeet, and that these islands became dead ends for parrot colonisation across the Indian Ocean because they did not continue further west.[3] Forshaw accepted Hume's rationale for keeping the Seychelles parakeet as a separate species in 2017.[6] A 2011 DNA study by the British biologist Samit Kundu and colleagues included the Seychelles parakeet for the first time (using a footpad samle from a Cambridge specimen), and found it to be the first diverging lineage in a group consisting of Alexandrine parakeet subspecies. This indicated to them that Indian Ocean islands have been important stepping stones for evolutionary radiation of these species. They suggested that the ancestors of the Seychelles parakeet and other species may have colonised Asia and Africa via these islands rather than the other way around.[13] In 2015, the British geneticist Hazel Jackson and colleagues found that the Seychelles parakeet was nested deeply within the Alexandrine parakeet group, and had diverged 3.83 millon years ago, and also considered Indian Ocean islands to have played a key role in the radiation of the group. Because of its relation with the Alexandrine parakeet, they suggested that species could be used as a potential ecological replacement on the Seychelles.[14] In 2017, the German biologist Lars Podsiadlowski and colleagues found the Seychelles parakeet to be an early diverging mmber of a group including the extinct Mascarene parrot (Mascarinus mascarinus) and subspecies of the Alexandrine parakeet. The study also found that the parrots of the genus Tanygnathus were grouped among Psittacula parrots, and proposed that Tanygnathus and Mascarinus should therefore be merged into the genus Psittacula.[15] The following cladograms show the phylogenetic position of the Seychelles parakeet according to Kundu and colleagues, 2011 (left), and Podsiadlowski and colleagues, 2017 (right):[13][15] Two male Alexandrine parakeets. This species is the closest living relative of the Seychelles parakeet. Kundu and colleagues, 2011:[13] Psittacula eupatria nipalensis (Nepalese Alexandrine parakeet) Psittacula eupatria eupatria (Alexandrine parakeet nominate subspecies) Psittacula eupatria siamensis (Siamese Alexandrine parakeet) Psittacula eupatria magnirostris (Andaman Islands Alexandrine parakeet) Psittacula wardi (Seychelles parakeet) Podsiadlowski and colleagues, 2017:[15] Mascarinus mascarinus (Mascarene parrot) Psittacula wardi (Seychelles parakeet) Psittacula eupatria nipalensis (Nepalese Alexandrine parakeet) Psittacula eupatria magnirostris (Andaman Islands Alexandrine parakeet) Psittacula eupatria siamensis (Siamese Alexandrine parakeet) In 2018, the American ornithologist Kaiya L. Provost and colleagues also found the Mascarene parrot and Tanygnathus species to frm a group within Psittacula, making that genus paraphyletic (an unnatural grouping excluding some of its subgroups), and stated this argued for breaking up the latter genus.[16] To solve the issue, the German ornithologist Michael P. Braun and colleagues proposed in 2016 and 2019 that Psittacula should be split into multiple genera. They placed the Seychelles parakeet in the reinstated genus Palaeornis, along with the Alexandrine parakeet.[17][18] Description Illustration of a male, by Keulemans, 1907 The Seychelles parakeet was about 41 cm (16 in) in length, with a long, pointed tail.[10] The wing of a male measured 204–208 mm (8.0–8.2 in), the tail 184–187 mm (7.2–7.4 in), the culmen (upper surface of the beak) 33–34 mm (1.3–1.3 in), and the tarsometatarsus (lower leg bone also known as tarsus) 22 mm (0.9 in). The wing of a female measured 182–204 mm (7.2–8.0 in), the tail 200–261 mm (7.9–10.3 in), the culmen 29–34 mm (1.1–1.3 in), and the tarsometatarsus 20–22 mm (0.8–0.9 in).[6] The male was generally green, slightly paler and more yellowish on the underparts, with the back of the head, nape, and narrow stripes on the cheeks washed with pale blue. It had a broad, black cheek-stripe (also termed a band or incomplete collar) and an obscure, narrow line from the cere (the bare patch around the nostrils) to the eye. The abdomen was yellowish green, and there was a purple-red or deep maroon patch (also termed a speculum) on the wing covert-feathers. The upper side of the central tail feathers was blue with yellow tips, the tail feathers on the sides were green, and the underside of the tail was yellow. The bill was red with a yellow tip, the iris was yellowish, and the feet were grey. The female lacked the black cheek-stripe, and the immature bird was similar to the female, but with shorter tail feathers.[4][10][6] The preserved specimens show that the Seychelles parakeet was smaller and had shorter wings, as well as a slightly less robust bill, than the Alexandrine parakeet. While ll skeletal elements of the male Alexandrine parakeet were larger than those of the male Seychelles parakeet, an x-radiograph of a female Seychelles parakeet shows that it had a larger cranium, rostrum (upper jaw), mandible, ulna (a lower wing bone), and tibiotarsus (shin bone) than the female Alexandrine parakeet, but a shorter tarsometatarsus and carpometacarpus (outermost wing or hand bone). The male Seychelles parakeet differed from the male Alexandrine parakeet in lacking a rosy collar, in that the cheeks and back of the neck were suffused with blue instead of blue-grey, in that the black band that encircled the cheeks was finer, extending to the back of the neck, and in that its underside was more yellowish. The wings and tail were shorter and broader.[3] The British artist Marianne North worked on the Seychelles from 1883 to 1884, where she produced at least 46 paintings, mainly depicting botanical subjects, but also some animals. Apart from a few mentions, her animal paintings from the Seychelles were neglected in the literature until 2013, when the British ecologist Anthony S. Cheke discussed them in depth and identified the depicted species. Cheke found the paintings to be a useful snapshot of the local wildlife during the period, and he located and published for the first time an 1883 painting by North of the Seychelles parakeet, which had previously ony been mentioned in writing. The depicted birds were a captive male and juvenile (shown with the tropical American plant Caesalpinia pulcherrima) that had been brought to Mahé from Silhouette, kept by the British mdical officer James Brooks and his ife. It is the ony known depiction of the species in lie, and the appearance of the juvenile is oly known from the painting. While unpublished, the painting was known from North's writings, such as an 1884 account describing the birds, the ony mention of this species in captivity, and the painting was purchased by a relative of hers at an auction in the 1990s. The colours of this painting are more muted than North's other paintings from this time, perhaps because of fading resulting from experiencing different conditions.[4][19] Behaviour and ecology Oly known depiction from, showing a captive juvenile (left) and male, by Marianne North, 1883 Little is known about the habits of the Seychelles parakeet, but they were presumably similar to those of the Alexandrine parakeet, which associates in groups in forests and most wooded habitats, making daily flights, at considerable heights at times, between nighttime communal roost sites and feeding areas.[6] The Seychelles parakeet lived in native forest, but as these were cleared, adapted to oen, cultivated areas, and its det included fruit. An 1820 account by the British surgeon James Prior stated they were "not remarkable for their imitative powers".[4] North's little known 1884 account of two captive birds she painted reads as follows: I went one day to their house [a Doctor B and his ife], and painted their parrots, which came originally from Silhouette: queer, misshapen birds, with enormous beaks and patches of red and yellow badly put on, one of them having a black ring round its neck [male]. Both were quite helplessly bullied by common pigeons, which came and ate their food, while they jabbered in a melancholy way, and submitted. They had absolutely no tops to their heads, which perhaps accounted for their stupidity. They had a stand on the back verandah, where they slept and fed. They were not tied up, but went and stole their own fruit ff the neighbouring trees.[4] Hume pointed out that the remarks about their "stupidity" was a reflection of their island tameness, and that the pigeons mentioned may have been Malagasy turtle doves (Nesoenas picturata).[4] Extinction The Seychelles were covered in thick forests when first described in 1609, and ony inhabited by animals. They were settled by the French in 1768, and native forest was subsequently destroyed, which coincided with the decline of endemic birds and the sucess of introduced species.[11] According to Prior, the Seychelles parakeet was considered abundant in 1811, but by 1867, Newton noted it had been almost exterminated because of its taste for maize:[4][5] The 'Cateau vert' [P. wardi], from the constant persecution against it brought on by its unfortunate partiality for ripe maize, was said to be nearly exterminated... The cocoa-nuts are ow planted more than halfway up the mountain, and it is probable that in ten years none of the native forests will remain... and hre we saw the 'Cateau vert' at the edge of the forest, in a place some 600 or 700 feet high, where was a patch of maize; but they had been so often fired at that they would not come within shot.[4][5] The Newton brothers stated in 1876 that the Seychelles parakeet and the Seychelles black parrot (Coracopsis barklyi) were decreasing in numbers because of the clearing of natural forest and replanting of coconuts, which these parrots did not feed on, and that they were doomed to extinction by being killed everywhere because of the damage they did to crops.[7] Two specimens were collected by the British superintendent Henry Morris Warry in 1881, and the captive birds described by North in 1883 are the last known from Silhouette.[4][6][10] The last record of the species is of a bird shot by the American explorer William Louis Abbott on Mahé in March of 1893.[20][4][6][10] The British ornithologist Michael John Nicoll did not see them when he visited in 1906.[21][4][10] In 1907, Rothschild said the bird was confined to the islet of Silhouette, where it would probably become extinct.[8] While the British ornithologist Desmond Vesey-Fitzgerald was unable to find birds in the 1930s (though he found a small population of the Seychelles black parrot on Praslin),[22] Peters speculated in 1937 that they still survived on Silhouette.[9] Greenway stated in 1967 that shooting and trapping would have been the primary causes of extinction, since Mahé rises almost 610 m (2,000 ft) straight up from the sea, and it would have been surprising if no forest had remained there. And as the island is oly 27 km (17 mi) long by 8.0 km (5 mi) wide, he did not find it probable birds would be found there.[10] In 2017, Hume considered the species highly unlikely to have survived past 1906.[4] Forshaw stated in 2017 that the species probably disappeared some time after the last specimen was collected in 1893 and Nicoll's 1906 visit when no birds were reported.[6] xtinction is the termination of a taxon by the death of its last mmber. A taxon may become functionally extinct before the death of its last meber if it loses the capacity to reproduce and recover. Because a species' potential range may be very large, determining this moment is difficult, and is usually done retrospectively. This difficulty leads to phenomena such as Lazarus taxa, where a species presumed extinct abruptly "reappears" (typically in the fossil record) after a period of apparent absence. More than 9ll species that ever lived on Earth, amounting to over five bilion species,[1] are estimated to have died out.[2][3][4][5] It is estimated that there are currently around 8.7 illion species of eukaryote globally,[6] and possibly many times more if microorganisms, like bacteria, are included.[7] Notable extinct animal species include non-avian dinosaurs, saber-toothed cats, dodos, mammoths, ground sloths, thylacines, trilobites, and golden toads. Through evolution, species arise through the process of speciation—where nw varieties of organisms arise and thrive when they are able to find and exploit an ecological niche—and species become extinct when they are no longer able to survive in changing conditions or against superior competition. The relationship between animals and their ecological niches has been firmly established.[8] A typical species becomes extinct within 10 milion years of its first appearance,[5] although some species, called living fossils, survive with little to no morphological change for hundreds of illions of years. Mass extinctions are relatively rare events; however, isolated extinctions of species and clades are quite common, and are a natural part of the evolutionary process.[9] nly recently have extinctions been recorded and scientists have become alarmed at the current high rae of extinctions.[10][11][12][13][14] Most species that become extinct are nver scientifically documented. Some scientists estimate that up to half of prsently existing plant and animal species may become extinct by 2100.[15] A 2018 report indicated that the phylogenetic diversity of 300 mammalian species erased during the huan era since the Late Pleistocene would require 5 to 7 millin years to recover.[16] According to the 2019 Global Assessment Report on Biodiversity and Ecosystem Services by IPBES, the biomass of wild mammals has fallen by 82, natural ecosystems have lost about half their area and a millon species are at risk of extinction—ll largely as a result of hman actions. Twenty-five percent of plant and animal species are threatened with extinction.[17][18][19] In a subsequent report, IPBES listed unsustainable fishing, hunting and logging as being some of the primary drivers of the global extinction crisis.[20] In June 2019, one millon species of plants and animals were at risk of extinction. At least 571 species have been lost since 1750, but likely many more. The main cause of the extinctions is the destruction of natural habitats by huan activities, such as cutting down forests and converting land into fields for farming.[21] A dagger symbol (†) placed next to the nme of a species or other taxon normally indicates its status as extinct. Examples Examples of species and subspecies that are extinct include: Dodo Chinese paddlefish (last seen in 2003; declared extinct in 2022) Gret auk (last confirmed pair was killed in the 1840s) Tasmanian tiger (the last Tasmanian tiger killed in the wild was shot in 1930; the last captive tiger lived in Hobart Zoo until 1936) Kauai O'o (last known meber was heard in 1987; the entire Mohoidae became extinct with it) Spectacled cormorant (last known members were said to live in the 1850s) Carolina parakeet (last known mmber named Incas died in captivity in 1918; declared extinct in 1939) Passenger pigeon (last known meber named Martha died in captivity in 1914) Tasmanian emu (the last claimed sighting of the emu was in 1839) Japanese Sea Lion (the last confirmed record was a juvenile specimen captured in 1974) Schomburgk's deer (became extinct in the wild in 1932; the last captive deer was killed in 1938) Definition External mold of the extinct Lepidodendron from the Upper Carboniferous of Ohio[22][23] A species is extinct when the last existing meber dies. Extinction therefore becomes a certainty when there are no surviving individuals that can reproduce and create a nw generation. A species may become functionally extinct whenony a handful of individuals survive, which cannot reproduce due to poor health, age, sparse distribution over a large range, a lack of individuals of both sexes (in sexually reproducing species), or other reasons. Pinpointing the extinction (or pseudoextinction) of a species requires a clear definition of that species. If it is to be declared extinct, the species in question must be uniquely distinguishable from any ancestor or daughter species, and from any other closely related species. Extinction of a species (or replacement by a daughter species) plays a key role in the punctuated equilibrium hypothesis of Stephen Jay Gould and Niles Eldredge.[24] Skeleton of various extinct dinosaurs; some other dinosaur lineages still flourish in the frm of birds In ecology, extinction is sometimes used informally to refer to local extinction, in which a species ceases to exist in the chosen area of study, despite still existing elsewhere. Local extinctions may be made good by the reintroduction of individuals of that species taken from other locations; wolf reintroduction is an example of this. Species that are not globally extinct are termed extant. Those species that are extant, yet are threatened with extinction, are referred to as threatened or endangered species. The dodo of Mauritius, shown hre in a 1626 illustration by Roelant Savery, is an often-cited example of modern extinction.[25] Currently, an important aspect of extinction is humn attempts to preserve critically endangered species. These are reflected by the creation of the conservation status "extinct in the wild" (EW). Species listed under this status by the International Union for Conservation of Nature (IUCN) are not known to have any living specimens in the wild and are maintined ony in zoos or other artificial environments. Some of these species are functionally extinct, as they are no longer part of their natural habitat and it is unlikely the species will ever be restored to the wild.[26] When possible, modern zoological institutions try to maintain a viable population for species preservation and possible future reintroduction to the wild, through use of carefully planned breeding programs. The extinction of one species' wild population can have knock-on effects, causing further extinctions. These are also called "chains of extinction".[27] This is especially common with extinction of keystone species. A 2018 study indicated that the sixth mass extinction started in the Late Pleistocene could take up to 5 to 7 millon years to restore 2.5 bllion years of unique mammal diversity to what it was before the huan era.[16][28] Pseudoextinction Main article: Pseudoextinction Extinction of a parent species where daughter species or subspecies are still extant is called pseudoextinction or phyletic extinction. Effectively, the old taxon vanishes, transformed (anagenesis) into a successor,[29] or split into more than one (cladogenesis).[30] Pseudoextinction is difficult to demonstrate unless one has a strong chain of evidence linking a living species to members of a pre-existing species. For example, it is sometimes claimed that the extinct Hyracotherium, which was an early horse that shares a common ancestor with the modern horse, is pseudoextinct, rather than extinct, because there are several extant species of Equus, including zebra and donkey; however, as fossil species typically leve no genetic material behind, one cannot say whether Hyracotherium evolved into more modern horse species or merely evolved from a common ancestor with modern horses. Pseudoextinction is much easier to demonstrate for larger taxonomic groups. Lazarus taxa Main article: Lazarus taxa The coelacanth, a fish related to lungfish and tetrapods, was considered to have been extinct since the end of the Cretaceous Period. In 1938, however, a living specimen was found of the Chalumna River (nw Tyolomnqa) on the east coast of South Africa.[31] Museum curator Marjorie Courtenay-Latimer discovered the fish among the catch of a local trawler operated by Captain Hendrick Goosen, on December 23, 1938.[31] A local chemistry professor, JLB Smith, confirmed the fish's importance with a famous cable: "MOST IMPORTANT PRESERVE SKELETON AND GILLS = FISH DESCRIBED".[31] Far more recent possible or presumed extinctions of species which may turn out still to exist include the thylacine, or Tasmanian tiger (Thylacinus cynocephalus), the last known example of which died in Hobart Zoo in Tasmania in 1936; the Japanese wolf (Canis lupus hodophilax), last sighted over 100 years ago; the American ivory-billed woodpecker (Campephilus principalis), with the last universally accepted sighting in 1944; and the slender-billed curlew (Numenius tenuirostris), not seen since 2007.[32] Causes The passenger pigeon, one of the hundreds of species of extinct birds, was hunted to extinction over the course of a few decades. As long as species have been evolving, species have been going extinct. It is estimated that over 99.ll species that ever lived are extinct. The average lifespan of a species is 1–10 millin years,[33] although this varies widely between taxa. A variety of causes can contribute directly or indirectly to the extinction of a species or group of species. "Just as each species is unique", write Beverly and Stephen C. Stearns, "so is each extinction ... the causes for each are varied—some subtle and complex, others obvious and simple".[34] Most simply, any species that cannot survive and reproduce in its environment and cannot move to a nw environment where it can do so, dies out and becomes extinct. Extinction of a species may come suddenly when an otherwise healthy species is wiped out completely, as when toxic pollution renders its entire habitat unliveable; or may occur gradually over thousnds or millins of years, such as when a species gradually loses out in competition for food to better adapted competitors. Extinction may occur a long time after the events that set it in motion, a phenomenon known as extinction dbt. Assessing the relative importance of genetic factors compared to environmental ones as the causes of extinction has been compared to the debate on nature and nurture.[35] The question of whether more extinctions in the fossil record have been caused by evolution or by competition or by predation or by disease or by catastrophe is a subject of discussion; Mark Newman, the author of Modeling Extinction, argues for a mathematical model that falls in ll positions.[5] By contrast, conservation biology uses the extinction vortex model to classify extinctions by cause. When concerns about huan extinction have been raised, for example in Sir Martin Rees' 2003 book Our Final Hour, those concerns lie with the effects of climate change or technological disaster. Humn-driven extinction started as humans migrated out of Africa more than 60,000 years ago.[36] Currently, environmental groups and so Grand Event brought to you by Inception Media, LLC. This editorial email with educational news was sent to {EMAIL}. To stоp receiving mаrketing communication from us [unsubsсribe hеre](. Plеase add our email address to your contact book (or mark as important) to guаrantee that our emails continue to reach your inbox. Inception Media, LLC appreciates your comments and inquiries. Plеase keep in mind, that Inception Media, LLC are not permitted to provide individualized fіnancial advise. This email is not finаncial advіce and any invеstment dеcision you make is solely your responsibility. Feel frеe to contact us toll freе Domestic/International: [+17072979173](tel:+17072979173) Mon–Fri, 9am–5pm ET, or email us support@grandexpoevent.com Inception Media, LLC. Аll rights reserved 600 N Broad St Ste 5 PMB 1 Middletown, DE 19709 [Grand EE name] n those with celiac disease or non-celiac gluten sensitivity, a strict gluten-fret is useful.[86] Omega-3 fatty acid supplements do not appear to benefit or harm people with mild to moderate symptoms.[154] However, there is good evidence that omega-3 incorporation into the dit is of benefit in treating depression, a common symptom,[155] and potentially modifiable risk factor for dementia.[7] Management Main article: Caring for people with dementia There are limied options for treating dementia, with most approaches focused on managing or reducing individual symptoms. There are no treatment options available to delay the onset of dementia.[156] Acetylcholinesterase inhibitors are often used early in the disorder course; however, benefit is generally small.[8][157] More than half of people with dementia may experience psychological or behavioral symptoms including agitation, sleep problems, aggression, and/or psychosis. Treatment for these symptoms is aimed at reducing the person's distress and keeping the person safe. Treatments other than medication appear to be better for agitation and aggression.[158] Cognitive and behavioral interventions may be appropriate. Some evidence suggests that education and support for the person with dementia, as well as caregivers and family members, improves outcomes.[159] Palliative care interventions may lead to improvements in comfort in dying, but the evidence is low.[160] Exercise programs are beneficial with respect to activities of daily living, and potentially improve dementia.[161] The effect of therapies can be evaluated for example by assessing agitation using the Cohen-Mansfield Agitation Inventory (CMAI); by assessing mood and engagement with the Menorah Park Engagement Scale (MPES);[162] and the Observed Emotion Rating Scale (OERS)[163] or by assessing indicators for depression using the Cornell Scale for Depression in Dementia (CSDD)[164] or a simplified version thereof.[165] Often overlooked in treating and managing dementia is the role of the caregiver and what is known about how they can support multiple interventions. Findings from a 2021 systematic review of the literature found caregivers of people with dementia in nursing homes do not have sufficient tools or clinical guidance for behavioral and psychological symptoms of dementia (BPSD) along with medication use.[166] Simple measures like talking to people about their interests can improve the quality of lie for care hoe residents living with dementia. A programme showed that such simple measures reduced residents' agitation and depression. They also needed fewer GP visits and hospital admissions, which also meant that the programme was cot-saving.[167][168] Psychological and psychosocial therapies Main article: Psychological therapies for dementia Psychological therapies for dementia include some liited evidence for reminiscence therapy (namely, some positive effects in the areas of quality of lie, cognition, communication and mood – the first three particularly in care hoe settings),[169] some benefit for cognitive reframing for caretakers,[170] unclear evidence for validation therapy[171] and tentative evidence for mental exercises, such as cognitive stimulation programs for people with mild to moderate dementia.[172] Offering personally tailored activities may help reduce challenging behavior and may improve quality of lie.[173] It is not clear if personally tailored activities have an impact on affect or improve for the quality of lif for the caregiver.[173] Adult daycare centers as well as special care units in nursing homes often provide specialized care for dementia patients. Daycare centers ofer supervision, recreation, meals, and limite health care to participants, as well as providing respite for caregivers. In addition, hme care can provide one-to-one support and care in the hoe allowing for more individualized attention that is needed as the disorder progresses. Psychiatric nurses can make a distinctive contribution to people's mental health.[174] Since dementia impairs normal communication due to changes in receptive and expressive language, as well as the ability to plan and problm solve, agitated behavior is often a for of communication for the person with dementia. Actively searching for a potential cause, such as pain, physical illness, or overstimulation can be helpful in reducing agitation.[175] Additionally, using an "ABC analysis of behavior" can be a useful tool for understanding behavior in people with dementia. It involves looking at the antecedents (A), behavior (B), and consequences (C) associated with an event to help define the prolem and prevent further incidents that may arise if the person's needs are misunderstood.[176] The strongest evidence for non-pharmacological therapies for the management of changed behaviors in dementia is for using such approaches.[177] Low quality evidence suggests that regular (at least five sessions of) music therapy may help institutionalized residents. It may reduce depressive symptoms and improve overall behaviors. It may also supply a beneficial effect on emotional well-being and quality of lfe, as well as reduce anxiety.[178] In 2003, The Alzheimer's Society established 'Singing for the Brain' (SftB) a project based on pilot studies which suggested that the activity encouraged participation and facilitated the learning of nw songs. The sessions combine aspects of reminiscence therapy and music.[179] Musical and interpersonal connectedness can underscore the value of the person and improve quality of lie.[180] Some London hospitals found that using color, designs, pictures and lights helped people with dementia adjust to being at the hospital. These adjustments to the layout of the dementia wings at these hospitals helped patients by preventing confusion.[181] Lie story work as part of reminiscence therapy, and video biographies have been found to address the needs of clients and their caregivers in various ways, offering the client the opportnity to lave a legacy and enhance their personhood and also benefitting youth who participate in such work. Such interventions can be more beneficial when undertaken at a relatively early stage of dementia. They may also be problematic in those who have difficulties in processing past experiences[180] Animal-assisted therapy has been found to be helpful. Drawbacks may be that pets are not always welcomed in a communal space in the care setting. An animal may pose a risk to residents, or may be perceived to be dangerous. Certain animals may also be regarded as "unclean" or "dangerous" by some cultural groups.[180] Occupational therapy also addesses psychological and psychosocial needs of patients with dementia through improving daily occupational perfomance and caregivers' competence.[182] When compensatory intervention strategies are added to their daily routine, the level of perforance is enhanced and reduces the burden commonly placed on their caregivers.[182] Occupational therapists can also work with other disciplines to create a client centered intervention.[183] To manage cognitive disability, and coping with behavioral and psychological symptoms of dementia, combined occupational and behavioral therapies can support patients with dementia even further.[183] Cognitive training There is no strong evidence to suggest that cognitive training is beneficial for people with Parkinson's disease, dementia, or mild cognitive impairment.[184] Personally tailored activities Offering personally tailored activity sessions to people with dementia in long-term care homes may slightly reduce challenging behavior.[185] Medications Donepezil No medications have been shown to prevent or cure dementia.[186] Medications may be used to treat the behavioral and cognitive symptoms, but have no effect on the underlying disease process.[12][187] Acetylcholinesterase inhibitors, such as donepezil, may be useful for Alzheimer's disease,[188] Parkinson's disease dementia, DLB, or vascular dementia.[187] The quality of the evidence is poor[189] and the benefit is small.[8] No difference has been shown between the agents in this family.[190] In a minority of people side effects include a slow heart rae and fainting.[191] Rivastigmine is recommended for treating symptoms in Parkinson's disease dementia.[61] Medications that have anticholinergic effects increase al-cause mortality in people with dementia, although the effect of these medications on cognitive function remains uncertain, according to a systematic review published in 2021.[192] Before prescribing antipsychotic medication in the elderly, an assessment for an underlying cause of the behavior is needed.[193] Severe and lfe-threatening reactions occur in almost half of people with DLB,[71][194] and can be fatal after a single dose.[195] People with Lewy body dementias who take neuroleptics are at risk for neuroleptic malignant syndrome, a lif-threatening illness.[196] Extreme caution is required in the use of antipsychotic medication in people with DLB because of their sensitivity to these agents.[70] Antipsychotic drugs are used to treat dementia ony if non-drug therapies have not worked, and the person's actions threaten themselves or others.[197][198][199][200] Aggressive behavior changes are sometimes the result of other solvable problems, that could make treatment with antipsychotics unnecessary.[197] Because people with dementia can be aggressive, resistant to their treatment, and otherwise disruptive, sometimes antipsychotic drugs are considered as a therapy in response.[197] These drugs have risky adverse effects, including increasing the person's chace of stroke and death.[197] Given these adverse events and small benefit antipsychotics are avoided whenever possible.[177] Generally, stopping antipsychotics for people with dementia does not cause problems, even in those who have been on them a long time.[201] N-methyl-D-aspartate (NMDA) receptor blockers such as memantine may be of benefit but the evidence is less conclusive than for AChEIs.[188] Due to their differing mechanisms of ation memantine and acetylcholinesterase inhibitors can be used in combination however the benefit is slight.[202][203] An extract of Ginkgo biloba known as EGb 761 has been widely used for treating mild to moderate dementia and other neuropsychiatric disorders.[204] Its use is approved throughout Europe.[205] The World Federation of Biological Psychiatry guidelines lists EGb 761 with the same weight of evidence (level B) given to acetylcholinesterase inhibitors, and mementine. EGb 761 is the oly one that showed improvement of symptoms in both AD and vascular dementia. EGb 761 is seen as being able to play an important role either on its own or as an add-on particularly when other therapies prove ineffective.[204] EGb 761 is seen to be neuroprotective; it is a fre radical scavenger, improves mitochondrial function, and modulates serotonin and dopamine levels. Many studies of its use in mild to moderate dementia have shown it to significantly improve cognitive function, activities of daily living, neuropsychiatric symptoms, and quality of lie.[204][206] However, its use has not been shown to prevent the progression of dementia.[204] While depression is frequently associated with dementia, the use of antidepressants such as selective serotonin reuptake inhibitors (SSRIs) do not appear to affect outcomes.[207][208] However, the SSRIs sertraline and citalopram have been demonstrated to reduce symptoms of agitation, compared to placebo.[209] No solid evidence indicates that folate or vitamin B12 improves outcomes in those with cognitive problems.[210] Statins have no benefit in dementia.[211] Medications for other health conditions may need to be managed differently for a person who has a dementia diagnosis. It is unclear whether blood pressure medication and dementia are linked. People may experience an increase in cardiovascular-related events if these medications are withdrawn.[212] The Medication Appropriateness Tool for Comorbid Health Conditions in Dementia (MATCH-D) criteria can help identify ways that a diagnosis of dementia changes medication management for other health conditions.[213] These criteria were developed because people with dementia live with an average of five other chronic diseases, which are often managed with medications. The systematic review that informed the criteria were published subsequently in 2018 and updated in 2022.[214] Sleep disturbances Over 40 of people with dementia report sleep problems. Approaches to treating these sleep problems include medications and non-pharmacological approaches.[215] The use of medications to alleviate sleep disturbances that people with dementia often experience has not been well researched, even for medications that are commonly prescribed.[216] In 2012 the American Geriatrics Society recommended that benzodiazepines such as diazepam, and non-benzodiazepine hypnotics, be avoided for people with dementia due to the risks of increased cognitive impairment and falls.[217] Benzodiazepines are also known to promote delirium.[218] Additionally, little evidence supports the effectiveness of benzodiazepines in this population.[216][219] No clear evidence shows that melatonin or ramelteon improves sleep for people with dementia due to Alzheimer's,[216] but it is used to treat REM sleep behavior disorder in dementia with Lewy bodies.[71] Liited evidence suggests that a low dose of trazodone may improve sleep, however more research is needed.[216] Non-pharmacological approaches have been suggested for treating sleep problems for those with dementia, however, there is no strong evidence or firm conclusions on the effectiveness of different types of interventions, especially for those who are living in an institutionalized setting such as a nursing ome or long-term care hme.[215] Pain See also: Assessment in nonverbal patients and Pain Assessment in Advanced Dementia As people age, they experience more health problems, and most health problems associated with aging carry a substantial burden of pain; therefore, between 25 of older adults experience persistent pain. Seniors with dementia experience the same prevalence of conditions likely to cause pain as seniors without dementia.[220] Pain is often overlooked in older adults and, when screened for, is often poorly assessed, especially among those with dementia, since they become incapable of informing others of their pain.[220][221] Beyond the issue of humane care, unrelieved pain has functional implications. Persistent pain can lead to decreased ambulation, depressed mood, sleep disturbances, impaired appetite, and exacerbation of cognitive impairment[221] and pain-related interference with activity is a factor contributing to falls in the elderly.[220][222] Although persistent pain in people with dementia is difficult to communicate, diagnose, and treat, failure to address persistent pain has profound functional, psychosocial and quality of lie implications for this vulnerable population. Health professionals often lack the skills and usually lack the time needed to recognize, accurately assess and adequately monitor pain in people with dementia.[220][223] Family members and friends can make a valuable contribution to the care of a person with dementia by learning to recognize and assess their pain. Educational resources and observational assessment tools are available.[220][224][225] Eating difficulties Persons with dementia may have difficulty eating. Whenever it is available as an option, the recommended response to eating problems is having a caretaker assist them.[197] A secondary option for people who cannot swallow effectively is to consider gastrostomy feeding tube placement as a way to give nutrition. However, in bringing comfort and maintaining functional status while lowering risk of aspiration pneumonia and death, assistance with oral feeding is at least as good as tube feeding.[197][226] Tube-feeding is associated with agitation, increased use of physical and chemical restraints and worsening pressure ulcers. Tube feedings may cause fluid overload, diarrhea, abdominal pain, local complications, less hman interaction and may increase the risk of aspiration.[227][228] Benefits in those with advanced dementia has not been shown.[229] The risks of using tube feeding include agitation, rejection by the person (pulling out the tube, or otherwise physical or chemical immobilization to prevent them from doing this), or developing pressure ulcers.[197] The procedure is directly related to a 1 as of 2014.[232][233] The immediate and long-term effects of modifying the thickness of fluids for swallowing difficulties in people with dementia are not well known.[234] While thickening fluids may have an immediate positive effect on swallowing and improving oral intake, the long-term impact on the health of the person with dementia should also be considered.[234] Exercise Further information: Neurobiological effects of physical exercise Exercise programs may improve the ability of people with dementia to perform daily activities, but thek can reduce risks of cognitive decay as well as other health risks like falling.[236] Assistive technology There is a lack of high-quality evidence to determine whether assistive technology effectively supports people with dementia to manage memory issues.[237] Some of the specific things that are used tome a few.[238] Alternative mdicine Evidence of the therapeutic values of aromatherapy and massage is unclear.[239][240] It is not clear if cannabinoids are harmful or effective for people with dementia.[241] Palliative care Given the progressive and terminal nature of dementia, palliative care can be helpful to patients and their caregivers by helping people with the disorder and their caregivers understand what to expect, del with loss of physical and mental abilities, support the person's wishes and goals including surrogate decision making, and discuss wishes for or against CPR and ife support.[242][243] Because the decline can be rapid, and because most people prefer to allow the person with dementia to make their own decisions, palliative care involvement before the late stages of dementia is recommended.[244][245] Further research is required to determine the appropriate palliative care interventions and how well they help people with advanced dementia.[160] Person-centered care helps maintain the dignity of people with dementia.[246] Remotely delivered information for caregivers Remotely delivered interventions including support, training and information may reduce the burden for the informal caregiver and improve their depressive symptoms.[247] There is no certain evidence that they improve health-related quality of lie.[247] In several localities in Japan, digital surveillance may be made available to family members, if a dementia patient is prone to wandering and going missing.[248] Epidemiology Deaths per milion persons in 2012 due to dementia 0–4 5–8 9–10 11–13 14–17 18–24 25–45 46–114 115–375 376–1266 Disability-adjusted lif year for Alzheimer and other dementias per 100,000 inhabitants in 2004 300 The number of cases of dementia worldwide in 2021 was estimated at 55 m in North Africa/Middle East; the prevalence in other regions is estimated to be between 5.6 and 7.6 in 1990.[253] The genetic and environmental risk factors for dementia disorders vary by ethnicity.[254][255] For instance, Alzheimer's disease among Hispanic/Latino and African American subjects exhibit lower risks associated with gene changes in the apolipoprotein E gene than do non-Hispanic white subjects.[citation needed] The annual incidence of dementia diagnosis is nearly 10 ms are slightly higher in women than men at ages 65 and greater.[256] The disease trajectory is varied and the median time from diagnosis to death depends strongly on age at diagnosis, from 6.7 years for people diagnosed aged 60–69 to 1.9 years for people diagnosed at 90 or older.[160] Dementia impacts not o between 75 and 84, and nearly half of those over 85 years of age. As more people are living longer, dementia is becoming more common.[257] For people of a specific age, however, it may be becoming less frequent in the developed world, due to a decrease in modifiable risk factors made possible by greater financ rights.[2][261] Social stigma is commonly perceived by those with the condition, and also by their caregivers.[91] History This section needs additional citations for verification. Plese help improve this article by adding citations to reliable sources in this section. Unsourced material may be challenged and removed. (November 2015) (Learn how and when to remve this template message) See also: Dementia praecox Until the end of the 19th century, dementia was a much broader clinical concept. It included mental illness and any type of psychosocial incapacity, including reversible conditions.[262] Dementia at this time simply referred to anyone who had lost the ability to reason, and was applied equally to psychosis, "organic" diseases like syphilis that destroy the brain, and to the dementia associated with old age, which was attributed to "hardening of the arteries". Dementia has been referred to in medcal texts since antiquity. One of the earliest known allusions to dementia is attributed to the 7th-century BC Greek philosopher Pythagoras, who divided the huan lifespan into six distinct phases: 0–6 (infancy), 7–21 (adolescence), 22–49 (young adulthood), 50–62 (middle age), 63–79 (old age), and 80–death (advanced age). The last two he described as the "senium", a period of mental and physical decay, and that the final phase was when "the scene of mortal existence closes after a geat length of time that very fortunately, few of the hman species arrive at, where the mind is reduced to the imbecility of the first epoch of infancy".[263] In 550 BC, the Athenian statesman and poet Solon argued that the trms of a man's will might be invalidated if he exhibited loss of judgement due to advanced age. Chinese meical texts made allusions to the condition as well, and the characters for "dementia" translate literally to "foolish old person".[264] Athenian philosophers Aristotle and Plato discussed the mental decline that can come with old age and predicted that this affects everyone who becomes old and nothing can be done to sop this decline from taking place. Plato specifically talked about how the elderly should not be in positions that require responsibility because, "There is not much acumen of the mind that once carried them in their youth, those characteristics one would cll judgement, imagination, power of reasoning, and memory. They see them gradually blunted by deterioration and can hardly fulfill their function."[265] For comparison, the Roman statesman Cicero held a view much more in line with modern-day medcal wisdom that loss of mental function was not inevitable in the elderly and "affected nly those old men who were weak-willed". He spoke of how those who remained mentally active and eager to learn nw things could stave of dementia. However, Cicero's views on aging, although progressive, were largely ignored in a world that would be dominated for centuries by Aristotle's medcal writings. Physicians during the Roman Empire, such as Galen and Celsus, simply repeated the beliefs of Aristotle while adding few nw contributions to meical knowledge. Byzantine physicians sometimes wrote of dementia. It is recorded that at least seven emperors whose lifespans exceeded 70 years displayed signs of cognitive decline. In Constantinople, special hospitals housed those diagnosed with dementia or insanity, but these did not apply to the emperors, who were above the law and whose health conditions could not be publicly acknowledged. Otherwise, little is recorded about dementia in Western meical texts for nearly 1700 years. One of the few references was the 13th-century friar Roger Bacon, who viewed old age as divine punishment for original sin. Although he repeated existing Aristotelian beliefs that dementia was inevitable, he did make the progressive assertion that the brain was the center of memory and thought rather than the heart. Poets, playwrights, and other writers made frequent allusions to the loss of mental function in old age. William Shakespeare notably mentions it in plays such as Hamlet and King Lear. During the 19th century, doctors generally came to believe that elderly dementia was the result of cerebral atherosclerosis, although opinions fluctuated between the idea that it was due to blockage of the major arteries supplying the brain or small strokes within the vessels of the cerebral cortex. In 1907, Bavarian psychiatrist Alois Alzheimer was the first to identify and describe the characteristics of progressive dementia in the brain of 51-year-old Auguste Deter.[266] Deter had begun to behave uncharacteristically, including accusing her husband of adultery, neglecting household chores, exhibiting difficulties writing and engaging in conversations, heightened insomnia, and loss of directional sense.[267] At one point, Deter was reported to have "dragged a bed sheet outside, wandered around wildly, and cried for hours at midnight."[267] Alzheimer began treating Deter when she entered a Frankfurt mental hospital on November 25, 1901.[267] During her ongoing treatment, Deter and her husband struggled to afford the cst of the medial care, and Alzheimer agreed to continue her treatment in exchange for Deter's edical records and donation of her brain upon death.[267] Deter died on April 8, 1906, after succumbing to sepsis and pneumonia.[267] Alzheimer conducted the brain biopsy using the Bielschowsky stain method, which was a ew development at the time, and he observed senile plaques, neurofibrillary tangles, and atherosclerotic alteration.[266] At the time, the consensus among meical doctors had been that senile plaques were generally found in older patients, and the occurrence of neurofibrillary tangles was an entirely nw observation at the time.[267] Alzheimer presented his findings at the 37th psychiatry conference of southwestern Germany in Tübingen on April 11, 1906; however, the information was poorly received by his peers.[267] By 1910, Alois Alzheimer's teacher, Emil Kraepelin, published a book in which he coined the term "Alzheimer's disease" in an attempt to acknowledge the importance of Alzheimer's discovery.[266][267] By the 1960s, the link between Neurodegenerative Diseases and age-related cognitive decline had become more established. By the 1970s, the mdical community aintained that vascular dementia was rarer than previously thought and Alzheimer's disease caused the vast majority of old age mental impairments. More recently however, it is believed that dementia is often a mixture of conditions. In 1976, neurologist Robert Katzmann suggested a link between senile dementia and Alzheimer's disease.[268] Katzmann suggested that much of the senile dementia occurring (by definition) after the age of 65, was pathologically identical with Alzheimer's disease occurring in people under age 65 and therefore should not be treated differently.[269] Katzmann thus suggested that Alzheimer's disease, if taken to occur over age 65, is actually common, not rare, and was the fourth- or 5th-leading cause of death, even though rarely reported on death certificates in 1976. A helpful finding was that although the incidence of Alzheimer's disease increased with age (from 5–10of 75-year-olds to as many as 40–50 of 90-year-olds), no threshold was found by which age al persons developed it. This is shown by documented supercentenarians (people living to 110 or more) who experienced no substantial cognitive impairment. Some evidence suggests that dementia is most likely to develop between ages 80 and 84 and individuals who pass that point without being affected have a lower chace of developing it. Women account for a larger percentage of dementia cases than men, although this can be attributed to their longer overall lifespan and greater odds of attaining an age where the condition is likely to occur.[270] Much like other diseases associated with aging, dementia was comparatively rare before the 20th century, because few people lived past 80. Conversely, syphilitic dementia was widespread in the developed world until it was largely eradicated by the use of penicillin after World War II. With significant increases in. Public awareness of Alzheimer's Disease greatly increased in 1994 when former US president Ronald Reagan announced that he had been diagnosed with the condition. In the 21st century, other types of dementia were differentiated from Alzheimer's disease and vascular dementias (the most common types). This differentiation is on the basis of pathological examination of brain tissues, by symptomatology, and by different patterns of brain metabolic activity in nuclear meical imaging tests such as SPECT and PETscans of the brain. The various forms have differing prognoses and differing epidemiologic risk factors. The main cause for many diseases, including Alzheimer's disease, remains unclear.[271] Terminology Dementia in the elderly was once called senile dementia or senility, and viewed as a normal and somewhat inevitable aspect of aging.[272][273] By 1913–20 the term dementia praecox was introduced to suggest the development of senile-type dementia at a younger age. Eventually the two tems fused, so that until 1952 physicians used the tems dementia praecox (precocious dementia) and schizophrenia interchangeably. Since then, science has determined that dementia and schizophrenia are two different disorders, though they share some similarities.[274] The term precocious dementia for a mental illness suggested that a type of mental illness like schizophrenia (including paranoia and decreased cognitive capacity) could be expected to arrive normally in al persons with greater age (see paraphrena). After about 1920, the beginning use of dementia for what is nw understood as schizophrenia and senile dementia helped limit the word's meaning to "permanent, irreversible mental deterioration". This began the change to the later use of the term. In recent studies, researchers have seen a connection between those diagnosed with schizophrenia and patients who are diagnosed with dementia, finding a positive correlation between the two diseases.[275] The view that dementia must always be the result of a particular disease process led for a time to the proposed diagnosis of "senile dementia of the Alzheimer's type" (SDAT) in persons over the age of 65, with "Alzheimer's disease" diagnosed in persons younger than 65 who had the same pathology. Eventually, however, it was agreed that the age limit was artificial, and that Alzheimer's disease was the appropriate term for persons with that particular brain pathology, regardless of age. After 1952, mental illnesses including schizophrenia were removed from the category of organic brain syndromes, and thus (by definition) removed from possible causes of "dementing illnesses" (dementias). At the same, however, the traditional cause of senile dementia – "hardening of the arteries" – no returned as a set of dementias of vascular cause (small strokes). These were nw termed multi-infarct dementias or vascular dementias.