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Lysosomal abnormalities in degenerating neurons link neuronal compromise to senile plaque development in Alzheimer disease

Cataldo, Anne M., Hamilton, Deborah J., Nixon, Ralph A.·1994·Brain Research
DOI 10.1016/0006-8993(94)91858-9
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Abstract

Antibodies to the lysosomal hydrolases, cathepsins B and D and beta-hexosaminidase A, revealed alterations of the endosomal-lysosomal system in neurons of the Alzheimer disease brain, which preceded evident degenerative changes and became marked as atrophy, neurofibrillary pathology, or chromatolysis developed. At the earliest stages of cell atrophy, hydrolase-positive lysosomes accumulated at the basal pole and then massively throughout the perikarya and proximal and proximal dendrites of affected pyramidal neurons in Alzheimer prefrontal cortex and hippocampus, far exceeding the changes of normal aging. Secondary lysosomes as well as tertiary residual bodies (lysosomes/lipofuscin) increased implying stimulated, autophagocytosis and lysosomal system activation. Less affected brain regions, such as the thalamus, displayed similar though less extensive alterations. Certain thalamic neurons exhibited a distinctive lysosome-related abnormality characterized by the presence of cell surface blebs of varying size and number filled with intense hydrolase immunoreactivity. At more advanced stages of degeneration in still intact neurons, hydrolase-positive lipofuscin, particularly in the form of abnormally large aggregates, nearly filled the cytoplasm. Similar lipofuscin aggregates were observed in abundance in the extracellular space following cell lysis and were usually associated with deposits of the beta-amyloid protein. Degenerating neurons and their processes were the major sour…

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  • Abnormal lysosomal positioning is a hallmark of Alzheimer's disease, with lysosomes accumulating in dystrophic axons around amyloid plaques.

    “Abnormal lysosomal positioning is a hallmark of Alzheimer's disease (AD), with lysosomes accumulating in dystrophic axons around amyloid plaques (Terry et al. 1964;Cataldo et al. 1994).”

    From TMEM55B downregulation promotes neurodegeneration in Alzheimer’s disease models (2026) · cites this paper as Cataldo et al. 1994

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Metadata

Authors
Cataldo, A. M., Hamilton, D. J., & Nixon, R. A.
Venue
Brain Research
Publisher
Elsevier BV
Published
1994-03
Volume
640
Issue
1-2
Pages
68-80
ISSN
0006-8993
DOI
10.1016/0006-8993(94)91858-9
Cited by
185
References
2
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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