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Abstract

We sought to determine the changes in the cholinergic pathways, which project from the nucleus basalis of Meynert (nBM) and travel in the subinsular region, in vascular dementia of the Binswanger type (VDBT) and Alzheimer's disease (AD). The subinsular regions were examined in 6 autopsied brains with VDBT, 5 brains with AD and 4 control brains without any neurologic diseases. The cholinergic pathway was labeled either by histochemistry for acetylcholine esterase (AChE), a degradatory enzyme of ACh, or by immunohistochemistry for choline acetyltransferase, its synthetic enzyme. The numerical density of nBM neurons did not differ significantly between these groups (163 +/- 49 in the VDBT, 105 +/- 82 in the AD and 198 +/- 76 in the control groups), but with a tendency towards a decrease in the AD group. The subinsular cholinergic fibers were impaired, with relative preservation of the nBM neurons in VDBT, whereas both the subinsular cholinergic fibers and the nBM neurons were degraded in AD. These results indicate that the cholinergic pathway is damaged not only in AD, but also in VDBT, and may further provide a pharmacological basis for treatment with AChE inhibitors in VDBT.

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Alzheimer disease: evidence for selective loss of cholinergic neurons in the nucleus basalis.

P J Whitehouse, D Price, A W Clark … (1981)

The nucleus basalis of Meynert provides diffuse cholinergic input to the neocortex. When compared with an age- and sex-matched control, the nucleus basalis from a patient with Alzheimer disease demonstrated substantial reduction of neurons. Loss of this neuronal population may represent an anatomical correlate of the well-documented cholinergic derangement in Alzheimer disease.

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Alzheimer's disease and senile dementia: loss of neurons in the basal forebrain

P. Whitehouse, D. Price, R. Struble … (1982)

Recent evidence indicates that the nucleus basalis of Meynert, a distinct population of basal forebrain neurons, is a major source of cholinergic innervation of the cerebral cortex. Postmortem studies have previously demonstrated profound reduction in the presynaptic markers for cholinergic neurons in the cortex of patients with Alzheimer's disease and senile dementia of the Alzheimer's type. The results of this study show that neurons of the nucleus basalis of Meynert undergo a profound (greater than 75 percent) and selective degeneration in these patients and provide a pathological substrate of the cholinergic deficiency in their brains. Demonstration of selective degeneration of such neurons represents the first documentation of a loss of a transmitter-specific neuronal population in a major disorder of higher cortical function and, as such, points to a critical subcortical lesion in Alzheimer's patients.