Histopathology of the Basal Forebrain and its Targets in Alzheimer Dementia

Abstract

The age-old problem of senility has been the subject of increasing scientific inquiry in recent years and for a good reason. When the proportion of aged individuals in a population rises, as is currently the situation in many Western societies, so does the incidence of age-related disorders. Prominent among these maladies have been diseases of the Alzheimer type, which have been estimated to account for approximately 60% of all senile dementias and for the vast majority of presenile dementias (Schneck et al., 1982). Although a “unified theory,” if such exists, of the etiology of Alzheimer dementias has yet to emerge, reasearch efforts have focused on various causal factors including increased aluminum concentrations in affected neurons, the presence of immunoglobulins, possible slow virus and/or subviral (prion) encephalopathies, microvasculature derangements, genetic susceptability, and involvement of specific neurotransmitter systems (for review, see Wurtman, 1985). In this report, we will concentrate on the role of one set of transmitter systems in the brain, namely those using acetylcholine as a chemical messenger, in the pathogenesis of Alzheimerfs disease (AD, clinical onset of symptoms before age 65) and senile dementia of the Alzheimer type (SDAT, clinical onset of symptoms at age 65 or later). In particular, we will consider the relationships between pathologic involvement of the basal forebrain cholinergic system in AD/SDAT and certain aspects of the clinical and classic neuropathologic profiles of those two disorders.