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Cited by 50Alzheimer's disease research and treatmentsCell death mechanisms and regulationDementia and Cognitive Impairment Research

Mechanisms of cell death in Alzheimer’s disease

Bancher, C., Lassmann, H., Breitschopf, H., Jellinger, K. A.·1997·Journal of Neural Transmission. Supplementa
DOI 10.1007/978-3-7091-6842-4_14
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Abstract

The etiology of Alzheimer's disease (AD) as well as its exact pathogenesis are unknown. Eventhough the deposition of beta A4 and the formation of neurofibrillary tangles represent impressive morphological hallmarks of the disease, several lines of evidence suggest that both lesions are not sufficient as causes of the neurodegenerative process. On the other hand, in vitro studies have shown that beta A4 is neurotoxic and is able to induce apoptotic cell death in neuronal cell cultures. Cells dying by apoptosis (programmed cell death) can be visualized in the tissue with a molecular biologic technique detecting fragmented nuclear DNA. Using this method, we have detected 50 x more neurons and 25 x more glial cells with nuclear DNA fragmentation in the brains of patients with AD than in non-demented controls. In contrast to previous studies, most of these cells did not reveal the characteristic morphological hallmarks of apoptosis. Most dying cells were not located within amyloid deposits and most dying cells did not bear a tangle. On the other hand, being in physical contact with an amyloid deposit increased the risk of a cell to dye by factor 5.7 and carrying a neurofibrillary tangle imposed a 3 times higher risk compared to unaffected nerve cells. Taken together, these data indicate that nerve cell death in AD occurs via a mechanism of programmed cell death different from classical apoptosis. Eventhough plaques and tangles increase the risk of cells to degenerate, both lesions are not the sole responsibles of the degenerative process, suggesting the existence of other factors that trigger the initiation of the cell death program in AD.

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Crossref · 10.1007/978-3-7091-6842-4_14

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62 of 62 references verified0 citation errors · 0 not checkable

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  • Aβ has been suggested as an initiator of neuronal death in AD by interaction with and disruption of ER and mitochondrial integrity and as a potential trigger of apoptosis.

    “Even though the exact mechanisms of neuronal death in AD are not yet fully understood, Aβ has been suggested as an initiator by interaction with and disruption of the endoplasmic reticulum (ER) and mitochondrial integrity [24] but also as a potential trigger of apoptosis [25].”

    From Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models (2020) · cites this paper as [25]

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Authors
Bancher, C., Lassmann, H., Breitschopf, H., & Jellinger, K. A.
Affiliations
University of Vienna (AT)
ORCID
Venue
Journal of Neural Transmission. Supplementa
Publisher
Springer Vienna
Published
1997
Volume
50
Pages
141-152
ISSN
0303-6995 (ISSN-L)
DOI
10.1007/978-3-7091-6842-4_14
OpenAlex
W2215207703
Cited by
50
References
62
Citations by year
2023: 1 · 2022: 2 · 2021: 2 · 2020: 3 · 2017: 1 · 2015: 2 · 2014: 1 · 2013: 1
FWCI
13.21
Type
book chapter
Language
en
Open access
closed
Locations
  • Journal of neural transmission. Supplementum (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, cell death mechanisms, apoptosis, amyloid-beta, neurofibrillary tangles, nuclear DNA fragmentation, neurodegeneration, amyloid plaques, glial cells, neuronal cell death
MeSH terms
Aged, Alzheimer Disease, Brain, Cell Nucleus, DNA, Humans, Nerve Degeneration, Nervous System Diseases, Reference Values, Artifacts, Neurofibrillary Tangles, Apoptosis

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