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Hypothesis linking plasticity, vulnerability and nerve growth factor to basal forebrain cholinergic neurons
Author(s) -
Perry Elaine K.
Publication year - 1990
Publication title -
international journal of geriatric psychiatry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.28
H-Index - 129
eISSN - 1099-1166
pISSN - 0885-6230
DOI - 10.1002/gps.930050404
Subject(s) - basal forebrain , nerve growth factor , neuroscience , cholinergic neuron , hippocampus , dementia , cholinergic , psychology , nucleus basalis , cerebral cortex , neurodegeneration , degenerative disease , disease , pathology , central nervous system disease , medicine , receptor
The hypothesis is advanced that two striking features of basal forebrain cholinergic neurons (BFCN)—their role in memory and their vulnerability in disease—are related to their dependence on nerve growth factor (NGF). Numerous studies, involving retrograde transport, receptor localization and responses to exogenous growth factor, have demonstrated a relatively selective association of NGF with these neurons in adult brain. The role of BFCN innervating cortical areas such as the hippocampus (and other cortical areas) in memory is widely supported by the results of surgical or pharmacological manipulation in experimental animals. Neuronal degeneration, indicated by decreased cortical cholinergic activity and/or subcortical cell loss, is also evident in a wide variety of cerebral disorders involving memory loss and dementia (Alzheimer's and Parkinson's disease, subacute sclerosing panencephalitis, Lewy body dementia and olivopontocerebellar atrophy are some examples) and to a lesser extent in normal ageing itself, in which memory is particularly vulnerable. Evidence is provided to support the idea that activity‐dependent uptake of NGF underlies both the memory function of BFCN and their susceptibility to disease. It is suggested that therapeutic strategies in dementia may need to be directed towards stimulation (pharmacological or physiological) of surviving BFCN.