title: [Does Alzheimer's disease exist in all primates? Alzheimer pathology in non-human primates and its pathophysiological implications (I)].
abstract: BACKGROUND
  Many publications consider that Alzheimer's disease (AD) is exclusive to the human species, and that no other animal species suffers from the disease. However, various studies have shown that some species can present with some of the defining characteristics of the human disease, including both neuropathological changes and cognitive-behavioural symptoms.
  
  
  METHODS
  In this work, the results published (PubMed) on senile brain changes in non-human primates of different degrees of evolution, are reviewed. The neuropathological changes associated with the accumulation of amyloid or highly phosphorylated tau protein are rare outside the primate order, but in all the sub-orders, families, genera and species of non-human primates that have been studied, some senile individuals have shown amyloid accumulation in the brain. In fact, in some species the presence of these deposits in senility is constant. Changes related to the accumulation of tau protein are always of very little significance, and have been detected only in some non-human primate species, both little evolved and highly evolved. In different species of non-human primates, some types of cognitive-behavioural changes are more common in some senile individuals when compared with both normal adult individuals and other senile individuals of the species. The importance of determining the longevity of the species in different habitats (natural habitats, new habitats, semi-captivity, captivity) is stressed in these studies.
  
  
  CONCLUSIONS
  Morphological, histochemical and cognitive-behavioural features similar to those observed in elderly humans are present in senile non-human primates. Moreover, other characteristics seen in non-human primates could be indicative of a pathological «Alzheimer type» ageing.
authors.affiliation: Instituto Cajal, CSIC, Madrid, España. atoledano@cajal.csic.es
authors.forename: A
authors.initials: A
authors.lastname: Toledano
authors.forename: M I
authors.initials: MI
authors.lastname: Alvarez
authors.forename: A B
authors.initials: AB
authors.lastname: López-Rodríguez
authors.forename: A
authors.initials: A
authors.lastname: Toledano-Díaz
authors.forename: C I
authors.initials: CI
authors.lastname: Fernández-Verdecia
mesh_terms: D000368:Aged; D000375:Aging / Q000502:physiology; D000544:Alzheimer Disease / Q000473:pathology* / Q000503:physiopathology / Q000523:psychology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D001519:Behavior / Q000502:physiology; D001522:Behavior, Animal / Q000502:physiology; D001921:Brain / Q000473:pathology; D003071:Cognition / Q000502:physiology; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D011323:Primates / Q000502:physiology*; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D016875:tau Proteins