Open AccessAged Non‐Human Primates: An Animal Model of Age‐Associated Neurodegenerative Disease
Author(s) -
Price Donald L.,
Martin Lee J.,
Sisodia Sangram S.,
Wagster Molly V.,
Koo Edward H.,
Walker Lary C.,
Koliatsos Vassilis E.,
Cork Linda C.
Publication year - 1991
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/j.1750-3639.1991.tb00672.x
Subject(s) - basal forebrain , neuroscience , cholinergic neuron , cholinergic , nerve growth factor , alzheimer's disease , nucleus basalis , disease , human brain , degenerative disease , psychology , biology , medicine , pathology , central nervous system disease , receptor
Aged non‐human primates develop age‐associated behavioral and brain abnormalities similar to those that occur in aged humans and, to a greater extent, in individuals with Alzheimer's disease. Declines in performance on cognitive and memory tasks begin at the monkey equivalent of late‐middle life. As occurs in elderly humans, significant differences have been demonstrated in levels of performance between animals within older age groups. The brains of old monkeys show degenerative changes in neurons, abnormal axons and neurites (particularly in telencephalic areas), and deposits of amyloid in senile plaques and around blood vessels. Moreover, in some older animals, decrements occur in markers of specific neurotransmitter circuits, including the basal forebrain cholinergic system. It has been suggested that alterations in these cholinergic neurons contribute to the memory deficits that occur in older individuals. Because axotomy‐induced retrograde degeneration of these neurons can be prevented by the administration of nerve growth factor, we have begun studies to determine whether administration of nerve growth factor improves performance of aged animals on memory tasks. This review describes the complementary nature of studies of non‐human primates and human subjects, illustrating how these investigations can clarify factors that influence behavior and brain biology in age‐associated diseases.