Neuronal Cell Death Mechanisms in Major Neurodegenerative Diseases
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Abstract
Neuronal cell death in the central nervous system has always been a challenging process to decipher. In normal physiological conditions, neuronal cell death is restricted in the adult brain, even in aged individuals. However, in the pathological conditions of various neurodegenerative diseases, cell death and shrinkage in a specific region of the brain represent a fundamental pathological feature across different neurodegenerative diseases. In this review, we will briefly go through the general pathways of cell death and describe evidence for cell death in the context of individual common neurodegenerative diseases, discussing our current understanding of cell death by connecting with renowned pathogenic proteins, including Tau, amyloid-beta, alpha-synuclein, huntingtin and TDP-43.
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Neuronal death or brain atrophy induced by amyloid, tau, and neuroinflammation might be prevented with neuroprotective therapies.
“Neuronal death or brain atrophy induced by amyloid, tau, and neuroinflammation might be prevented with neuroprotective therapies, which include suppressing excitable amino acid signaling pathways, free radical scavengers, and regeneration enhancers (Table 3) [29].”
From Clinical trials of new drugs for Alzheimer disease (2020) · cites this paper as [29]
Section 3.2 links amyloid-beta and Tau to neuronal death, and the Introduction and Future Directions discuss developing treatments to counter disease progression. But the copy does not support the full attributed claim: it does not identify neuroinflammation as a cause in this account or describe the listed neuroprotective therapies—suppressing excitatory amino acid signaling, free-radical scavengers, and regeneration enhancers—as ways to prevent neuronal death or brain atrophy. No page numbers are provided for these passages. (LLM, conf=0.84)
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- Authors
- Chi, H., Chang, H.-Y., & Sang, T.-K.
- Affiliations
- National Tsing Hua University (TW)
- Corresponding author
- Chang, Hui-Yun
- Sang, Tzu-Kang
- ORCID
- Sang, Tzu-Kang
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2018-10-09
- Volume
- 19
- Issue
- 10
- Pages
- 3082
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC6213751
- OpenAlex
- W2897537084
- Cited by
- 412
- References
- 16
- Citations by year
- 2026: 30 · 2025: 68 · 2024: 78 · 2023: 70 · 2022: 70 · 2021: 45 · 2020: 33 · 2019: 16 · 2018: 2
- FWCI
- 2.38
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Preprints.org (acceptedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Ministry of Science and Technology, Taiwan (107-2311-B-007-006, 106-2311-B-007-008-MY3)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- neuronal cell death, neurodegenerative diseases, cell death pathways, tau protein, amyloid-beta, alpha-synuclein, huntingtin, TDP-43, pathogenic proteins, central nervous system
- MeSH terms
- Animals, Brain, Humans, Neurons, Cell Death, Apoptosis, Neurodegenerative Diseases
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