title: [Does Alzheimer's disease exist in all primates? Alzheimer pathology in non-human primates and its pathophysiological implications (II)].
abstract: BACKGROUND
  In the ageing process there are some species of non-human primates which can show some of the defining characteristics of the Alzheimer's disease (AD) of man, both in neuropathological changes and cognitive-behavioural symptoms. The study of these species is of prime importance to understand AD and develop therapies to combat this neurodegenerative disease.
  
  
  METHODS
  In this second part of the study, these AD features are discussed in the most important non-experimental AD models (Mouse Lemur -Microcebus murinus, Caribbean vervet -Chlorocebus aethiops, and the Rhesus and stump-tailed macaque -Macaca mulatta and M. arctoides) and experimental models (lesional, neurotoxic, pharmacological, immunological, etc.) non-human primates. In all these models cerebral amyloid neuropathology can occur in senility, although with different levels of incidence (100% in vervets;<30% in macaques). The differences between normal and pathological (Alzheimer's) senility in these species are difficult to establish due to the lack of cognitive-behavioural studies in the many groups analysed, as well as the controversy in the results of these studies when they were carried out. However, in some macaques, a correlation between a high degree of functional brain impairment and a large number of neuropathological changes ("possible AD") has been found.
  
  
  CONCLUSIONS
  In some non-human primates, such as the macaque, the existence of a possible continuum between "normal" ageing process, "normal" ageing with no deep neuropathological and cognitive-behavioural changes, and "pathological ageing" (or "Alzheimer type ageing"), may be considered. In other cases, such as the Caribbean vervet, neuropathological changes are constant and quite marked, but its impact on cognition and behaviour does not seem to be very important. This does assume the possible existence in the human senile physiological regression of a stable phase without dementia even if neuropathological changes appeared.
authors.affiliation: Instituto Cajal, CSIC, Madrid, España. Electronic address: atoledano@cajal.csic.es.
authors.forename: A
authors.initials: A
authors.lastname: Toledano
authors.affiliation: Instituto Cajal, CSIC, Madrid, España.
authors.forename: M I
authors.initials: MI
authors.lastname: Álvarez
authors.affiliation: Instituto Cajal, CSIC, Madrid, España.
authors.forename: A B
authors.initials: AB
authors.lastname: López-Rodríguez
authors.affiliation: Departamento de Reproducción Animal, INIA, Madrid, España.
authors.forename: A
authors.initials: A
authors.lastname: Toledano-Díaz
authors.affiliation: Centro Internacional de Restauración Neurológica (CIREN), Cubanacán, La Habana, Cuba.
authors.forename: C I
authors.initials: CI
authors.lastname: Fernández-Verdecia
mesh_terms: D000544:Alzheimer Disease / Q000473:pathology*; D000818:Animals; D006801:Humans; D018419:Primate Diseases / Q000473:pathology*; D011323:Primates