Dendritic reorganisation in the basal forebrain under degenerative conditions and its defects in Alzheimer's disease. II. Ageing, Korsakoff's disease, Parkinson's disease, and Alzheimer's disease.
Changes in the dendritic arborisation of Golgi-impregnated basal forebrain neurones with respect to size, shape, orientation, and topology of branching were quantitatively investigated in ageing, Alzheimer's disease (AD), Korsakoff's disease (KD), and Parkinson's disease (PD). A reorganisation of the whole dendritic tree characterized by an increase in both the total dendritic length and the degree of dendritic arborisation as well as by changes in the shape of the dendritic field was found during ageing, in KD, PD, and AD. Dendritic growth under these conditions was related to the extent of cell loss in basal forebrain nuclei. There appeared to be major differences, however, with respect to the overall pattern of dendritic reorganisation between AD on one side and ageing, KD, and PD on the other side. In both ageing and KD, dendritic growth was largely restricted to the terminal dendritic segments, resulting in an increase of the size of the dendritic field (pattern of "extensive growth") In AD, however, dendritic growth mainly resulted in an increase of the dendritic density within the dendritic field without being accompanied by an increase in the size of the volume occupied by the dendritic tree (pattern of "intensive growth"). In AD, aberrant growth processes were frequently observed in the perisomatic area or on distal dendritic segments of basal forebrain neurones of the reticular type. Neurones with aberrant growth profiles were typically located in the direct vicinity of deposits of beta/A4 amyloid. Perisomatic growth profiles were covered by the low-affinity receptor of nerve growth factor p75NGFR. Aberrant growth processes were not present in ageing, KD, and PD. On the basis of the present study, it is concluded that under certain degenerative conditions, reticular basal forebrain neurones undergo a compensatory reorganisation of their dendritic arborisation, a process that has become defective in AD, thereby converting a physiological signal into a cascade of events contributing to the pathology of the disease.
Arendt
T
T
Department of Neurochemistry, Paul Flechsig Institute of Brain Research, University of Leipzig, Germany.
Brückner
M K
MK
Bigl
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Marcova
L
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D000328:Adult; D000368:Aged; D000375:Aging / Q000473:pathology*; D000425:Alcohol Amnestic Disorder / Q000473:pathology*; D000544:Alzheimer Disease / Q000473:pathology*; D052160:Benzothiazoles; D002452:Cell Count; D003712:Dendrites / Q000502:physiology*; D005260:Female; D005456:Fluorescent Dyes; D006651:Histocytochemistry; D006801:Humans; D008297:Male; D008875:Middle Aged; D009410:Nerve Degeneration / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D010300:Parkinson Disease / Q000473:pathology*; D016548:Prosencephalon / Q000473:pathology*; D013194:Staining and Labeling; D013844:Thiazoles
D052160:Benzothiazoles; D005456:Fluorescent Dyes; D013844:Thiazoles; C009462:thioflavin T