CHOLINERGIC INNERVATION OF THE AMYGDALOID COMPLEX IN THE HUMAN BRAIN AND ITS ALTERATIONS IN OLD-AGE AND ALZHEIMERS-DISEASE

The cholinergic innervation of the human amygdaloid complex was studie d immunohistochemically with a choline acetyltransferase (ChAT) antibo dy in eight brains: five control and three with Alzheimer's disease (A D). All amygdaloid nuclei displayed ChAT-immunopositive axons and vari cosities. The density of these axons reached levels that were higher t han in any other part of the forebrain except for the striatum. The hi ghest level of ChAT-immunopositive profiles was seen in the basolatera l nucleus and the second highest in the lateral part of the central nu cleus. The basomedial, accessory basal, and cortical nuclei, the amygd alo-hippocampal and cortico-amygdaloid transition areas, as well as th e anterior amygdaloid area, showed a moderate density of ChAT-positive varicosities and fibers. The lateral nucleus displayed a relatively l ow density of cholinergic innervation, and there were only rare ChAT-p ositive fibers in the medial nucleus. Although the level of cholinergi c innervation in the lateral nucleus was relatively lower than in many of the other amygdaloid nuclei, it was approximately equivalent to th at of entorhinal cortex, a region that receives one of the heaviest ch olinergic inputs in the cerebral cortex. The distribution of the choli nergic fibers as studied by ChAT immunohistochemistry was nearly ident ical to that observed with AChE histochemistry. Quantitative densitome try in control specimens showed that there was no decline of amygdaloi d cholinergic input when middle-aged subjects were compared with senes cent subjects. In AD there was a severe and regionally selective deple tion of this innervation in the amygdaloid complex. The cortical, acce ssory basal, and lateral nuclei displayed the most severe loss of ChAT -positive profiles, whereas the basolateral, and especially the centra l, nuclei displayed relatively little change. There was no consistent relationship between the loss of cholinergic fibers and the density of amyloid plaques and neurofibrillary tangles in amygdaloid nuclei. (C) 1993 Wiley-Liss, Inc.