Differing patterns of aberrant neuronal sprouting in Alzheimer's disease with and without Lewy bodies
| Autor: | Eliezer Masliah, Richard DeTeresa, M. Alford, Margaret Mallory, Lawrence A. Hansen |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
Pathology
medicine.medical_specialty Neurofilament Hippocampus Nerve Tissue Proteins Amyloid beta-Protein Precursor GAP-43 Protein Degenerative disease Alzheimer Disease Neurites Amyloid precursor protein medicine Humans Senile plaques Gap-43 protein Growth Substances Molecular Biology Aged Neurons Membrane Glycoproteins biology Lewy body General Neuroscience medicine.disease Immunohistochemistry Synapses biology.protein Lewy Bodies Neurology (clinical) Alzheimer's disease Neuroscience Developmental Biology |
| Zdroj: | Brain Research. 617:258-266 |
| ISSN: | 0006-8993 |
| DOI: | 10.1016/0006-8993(93)91093-8 |
| Popis: | About one quarter of Alzheimer's disease patients have been found to have concomitant subcortical and neocortical Lewy bodies (LBs). We compared the aberrant neuronal sprouting and the extent of neuritic and synaptic damage in these Lewy body variant of Alzheimer's disease (LBV), with the same pathologic alterations in Alzheimer's disease without LBs (AD). More of the thioflavine-S-positive senile plaques of the LBVs contained growth associated protein 43 (GAP-43), a marker of neuritic growth and sprouting. Compared to AD, the LBVs had 39% more GAP-43-positive plaques in the frontal cortex, and 53% more in the hippocampus. These neuritic alterations were accompanied by an accumulation of amyloid precursor protein and phosphorylate neurofilaments.. Synapse loss was the same in LBV and AD. These results suggest more extensive aberrant neuronal sprouting in LBV than in AD. |
| Databáze: | OpenAIRE |
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