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      Loss of neurons in the nucleus basalis of Meynert in Alzheimer's disease, paralysis agitans and Korsakoff's disease

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      Acta Neuropathologica

      Springer Nature

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

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

            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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              Observations on the brains of demented old people.

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                Author and article information

                Journal
                Acta Neuropathologica
                Acta Neuropathol
                Springer Nature
                0001-6322
                1432-0533
                1983
                1983
                : 61
                : 2
                : 101-108
                Article
                10.1007/BF00697388
                © 1983
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