The DOI matches its Crossref record; 329 of the 329 references it cites were found in a registry or an index.
The cause of neuronal degeneration in Alzheimer’s disease
Open accessAbstract
Alzheimer's disease is associated with a specific pattern of pathological changes in the brain that result in neurodegeneration and the progressive development of dementia. Pathological hallmarks common to the disease include beta-amyloid plaques, dystrophic neurites associated with plaques and neurofibrillary tangles within nerve cell bodies. The exact relationship between these pathological features has been elusive, although it is clear that beta-amyloid plaques precede neurofibrillary tangles in neocortical areas. Examination of the brains of individuals in the preclinical stage of the disease have shown that the earliest form of neuronal pathology associated with beta-amyloid plaques resembles the cellular changes that follow structural injury to axons. Thus, the development of beta-amyloid plaques in the brain may cause physical damage to axons, and the abnormally prolonged stimulation of the neuronal response to this kind of injury ultimately results in the profound cytoskeletal alterations that underlie neurofibrillary pathology and neurodegeneration. Therapeutically, inhibition of the neuronal reaction to physical trauma may be a useful neuroprotective strategy in the earliest stages of Alzheimer's disease.
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“The pathology of AD manifests with degeneration of the neurons, along with loss of synapses in the cortex, the hippocampus, and the subcortical structures [12].”
From The Multifaceted Role of Neuroprotective Plants in Alzheimer’s Disease Treatment (2022) · cites this paper as [12]
Citations
Cites
Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123
Corder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., Roses, A. D., Haines, J. L., & Pericak-Vance, M. A. (1993) · Science · doi:10.1126/science.8346443 · Cited by 9,429
Alzheimer's disease: the amyloid cascade hypothesis
Hardy, J. A., & Higgins, G. A. (1992) · Science · doi:10.1126/science.1566067 · Cited by 7,484
Glenner, G. G., & Wong, C. W. (1984) · Biochemical and Biophysical Research Communications · doi:10.1016/s0006-291x(84)80190-4 · Cited by 5,404
Mirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961
Amyloid plaque core protein in Alzheimer disease and Down syndrome.
Masters, C. L., Simms, G., Weinman, N. A., Multhaup, G., McDonald, B. L., & Beyreuther, K. (1985) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.82.12.4245 · Cited by 4,431
Apolipoprotein E: Cholesterol Transport Protein with Expanding Role in Cell Biology
Mahley, R. W. (1988) · Science · doi:10.1126/science.3283935 · Cited by 4,028
Diffusible, nonfibrillar ligands derived from Aβ 1–42 are potent central nervous system neurotoxins
Lambert, M. P., Barlow, A. K., Chromy, B. A., Edwards, C., Freed, R., Liosatos, M., Morgan, T. E., Rozovsky, I., Trommer, B., Viola, K. L., et al. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.11.6448 · Cited by 3,506
Degeneration and Regeneration of the Nervous System.
(1929) · JAMA · doi:10.1001/jama.1929.02710220063037 · Cited by 2,908
The molecular pathology of Alzheimer's disease
Selkoe, D. J. (1991) · Neuron · doi:10.1016/0896-6273(91)90052-2 · Cited by 2,708
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The role of oxidative stress in the toxicity induced by amyloid β-peptide in Alzheimer’s disease
Miranda, S., Opazo, C., Larrondo, L. F., Muñoz, F. J., Ruiz, F., Leighton, F., & Inestrosa, N. C. (2000) · Progress in Neurobiology · doi:10.1016/s0301-0082(00)00015-0 · Cited by 369
Lockhart, A., Ye, L., Judd, D. B., Merritt, A. T., Lowe, P. N., Morgenstern, J. L., Hong, G., Gee, A. D., & Brown, J. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m412056200 · Cited by 213
Does Alzheimer's disease begin in the brainstem?
Simic, G., Stanic, G., Mladinov, M., Jovanov‐Milosevic, N., Kostovic, I., & Hof, P. R. (2009) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2009.01038.x · Cited by 204
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Interneurons, tau and amyloid-β in the piriform cortex in Alzheimer’s disease
Saiz-Sanchez, D., De la Rosa-Prieto, C., Ubeda-Banon, I., & Martinez-Marcos, A. (2015) · Brain Structure and Function · doi:10.1007/s00429-014-0771-3 · Cited by 79
Schnurra, I., Bernstein, H.-G., Riederer, P., & Braunewell, K.-H. (2001) · Neurobiology of Disease · doi:10.1006/nbdi.2001.0432 · Cited by 76
Axonopathy and cytoskeletal disruption in degenerative diseases of the central nervous system
Vickers, J. C., King, A. E., Woodhouse, A., Kirkcaldie, M. T., Staal, J. A., McCormack, G. H., Blizzard, C. A., Musgrove, R. E. J., Mitew, S., Liu, Y., et al. (2009) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2009.08.004 · Cited by 69
Self-citationIs mitochondrial DNA depletion involved in Alzheimer's disease?
Rodríguez-Santiago, B., Casademont, J., & Nunes, V. (2001) · European Journal of Human Genetics · doi:10.1038/sj.ejhg.5200629 · Cited by 57
Exercise-Induced Modulation of Neuroinflammation in Models of Alzheimer’s Disease
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The Multifaceted Role of Neuroprotective Plants in Alzheimer’s Disease Treatment
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“The pathology of AD manifests with degeneration of the neurons, along with loss of synapses in the cortex, the hippocampus, and the subcortical structures [12].”
Background
Metadata
- Authors
- Vickers, J.
- Affiliations
- University of Tasmania (AU)
- Corresponding author
- Vickers, J
- ORCID
- Vickers, J
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2000-02
- Volume
- 60
- Issue
- 2
- Pages
- 139-165
- ISSN
- 0301-0082 (ISSN-L)
- OpenAlex
- W2111417422
- Cited by
- 254
- References
- 329
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 9 · 2023: 7 · 2022: 7 · 2021: 7 · 2020: 6 · 2019: 6 · 2018: 4 · 2017: 7 · 2016: 3 · 2015: 6 · 2014: 12 · 2013: 6 · 2012: 7
- FWCI
- 12.98
- Type
- journal article
- Language
- en
- Open access
- green
- figshare.com
- Licence
- Locations
- Progress in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- eCite Digital Repository (University of Tasmania) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, neurodegeneration, amyloid plaques, neurofibrillary tangles, dystrophic neurites, axonal injury, cytoskeletal alterations, dementia, neuroprotection, preclinical Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Animals, Humans, Nerve Degeneration
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