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
- 9 January 1995
- journal article
- research article
- Published by Wiley in Journal of Comparative Neurology
- Vol. 351 (2) , 189-222
- https://doi.org/10.1002/cne.903510203
Abstract
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, 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 β/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. © 1995 Willy-Liss, Inc.Keywords
This publication has 186 references indexed in Scilit:
- Alzheimer Disease Brain Extract Stimulates Branching of Laminin-Mediated Neuronal ProcessesAlzheimer Disease & Associated Disorders, 1992
- Neuropathological stageing of Alzheimer-related changesActa Neuropathologica, 1991
- Basic fibroblast growth factor in Alzheimer's diseaseBiochemical and Biophysical Research Communications, 1990
- Fibroblast growth factor induces β-amyloid precursor mRNA in glial but not neuronal cultured cellsBiochemical and Biophysical Research Communications, 1990
- Developmental and differential expression of beta amyloid protein precursor mRNAs in mouse brainBiochemical and Biophysical Research Communications, 1990
- Amyloid beta protein precursor is a mitogenBiochemical and Biophysical Research Communications, 1989
- Alcohol withdrawal does not impede hippocampal granule cell progressive loss in chronic alcohol-fed ratsNeuroscience Letters, 1988
- Quantitative changes in morphological parameters in the developing visual cortex of the marmoset monkeyDevelopmental Brain Research, 1986
- NGF-Mediated increase of choline acetyltransferase (ChAT) in the neonatal rat forebrain: Evidence for a physiological role of NGF in the brain?Developmental Brain Research, 1983
- ParkinsonismNeurology, 1967