Regional neuronal loss in aging and Alzheimer's disease: a brief review
Open accessAbstract
It is widely recognized that regional neuronal loss occurs during normal aging and that excessive neuronal loss in specific regions is one hallmark of Alzheimer's disease (AD). Modern counting techniques have started to better define the degree of neuronal loss in aging and AD. Although there is some overlap with regions affected during aging, it is clear that Alzheimer's disease represents a specific entity. By determining the regions and types of neurons that are vulnerable we can hope to better understand the causes and processes of normal aging and Alzheimer's disease, as well as develop potential therapies.
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Functionally distinct brain areas display significant differences in neuronal loss despite overall low rate of neuronal death during adulthood.
“Despite the overall low rate of neuronal death during adulthood, functionally distinct brain areas display significant differences in neuronal loss2.”
From Epigenetic regulation of brain region-specific microglia clearance activity (2018) · cites this paper as [2]
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“, 2003), early stages of AD (O’Banion et al., 1994), chronic epileptic seizures (Mathern et al.”
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BackgroundEpigenetic regulation of brain region-specific microglia clearance activity
Ayata, P., Badimon, A., Strasburger, H. J., Duff, M. K., Montgomery, S. E., Loh, Y.-H. E., Ebert, A., Pimenova, A. A., Ramirez, B. R., Chan, A. T., et al. (2018) · Nature Neuroscience · doi:10.1038/s41593-018-0192-3 · Cited by 460 · see citing works
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“Moreover, earlier and recent studies have shown a neuronal reduction in temporal, inferior and superior parietal and frontal cortices of AD cases [35,36].”
ResultFunctional Genomics of Brain Aging and Alzheimers Disease: Focus on Selective Neuronal Vulnerability
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“For example, in the hippocampus, neurons in the CA1 region are vulnerable to brain aging and AD, but those in the nearby CA3 region are not nearly as heavily damaged as the CA1 neurons [1-3].”
BackgroundWang, X., Zaidi, A., Pal, R., Garrett, A. S., Braceras, R., Chen, X., Michaelis, M. L., & Michaelis, E. K. (2009) · BMC Neuroscience · doi:10.1186/1471-2202-10-12 · Cited by 84 · see citing works
“CA3 neurons has been observed following episodes of global cerebral ischemia [11,46], early phases of Alzheimer's disease [47], chronic epileptic seizures [48], and OS [5,20].”
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Self-citationGene expression profiles in microdissected neurons from human hippocampal subregions
Torres-Muñoz, J., van Waveren, C., Keegan, M. G., Bookman, R. J., & Petito, C. K. (2004) · Molecular Brain Research · doi:10.1016/j.molbrainres.2004.05.017 · Cited by 58 · see citing works
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“Although there are more than 100 transgenic mouse models that each capture certain aspects of AD [9], 5xFAD mice can uniquely model neuronal loss [9] and sex-specific amyloid pathology, both of which are well-established observations in AD patients [10,11].”
BackgroundCortical Neuropathology in Aging and Dementing Disorders
Hof, P. R., Bouras, C., & Morrison, J. H. (1999) · Cerebral cortex · doi:10.1007/978-1-4615-4885-0_8 · Cited by 35 · see citing works
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Decreased Expression of Prostaglandin G/H Synthase-2 (PGHS-2) in Alzheimer’s Disease Brain
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Self-citationGlial and Neuronal Expression of Cyclooxygenase-2: Relevance to Alzheimer’S Disease
O’Banion, M. K., Chang, J. W., Kaplan, M. D., Yermakova, A., & Coleman, P. D. (1997) · Advances in experimental medicine and biology · doi:10.1007/978-1-4899-1810-9_36 · Cited by 8 · see citing works
Self-citationMurphy, S. A., Chen, L., Doherty, J. M., Acharyya, P., Riley, N., Johnson, A. M., Walker, A. I. B., Domash, H., Jorgensen, M., Bayat, S., et al. (2022) · Frontiers in Psychology · doi:10.3389/fpsyg.2022.1076735 · Cited by 5 · see citing works
“As we age, neuronal loss results in atrophy of areas like the hippocampus and cortical regions (O’banion et al., 1994; Morrison and Hof, 1997).”
BackgroundLongevity and Brain Aging: The Paradigm of Centenarians
Bouras, C., Vallet, P. G., Kövari, E., Michel, J., Herrmann, F. R., Hof, P. R., & Giannakopoulos, P. (2001) · Elsevier eBooks · doi:10.1016/b978-012351830-9/50010-x
Pathak, A. K., & Singh, B. (2023) · Research Square · doi:10.21203/rs.3.rs-2578348/v1
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- Authors
- O'Banion, M. K., Coleman, P. D., & Callahan, L. M.
- Affiliations
- University of Rochester Medicine (US)
- Venue
- Seminars in Neuroscience
- Publisher
- Elsevier BV
- Published
- 1994-10
- Volume
- 6
- Issue
- 5
- Pages
- 307-314
- ISSN
- 1044-5765 (ISSN-L)
- OpenAlex
- W2105790396
- Cited by
- 23
- References
- 0
- Citations by year
- 2024: 1 · 2023: 3 · 2022: 1 · 2018: 2 · 2015: 2
- FWCI
- 0.89
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Seminars in Neuroscience (publishedVersion, cc-by-nc-nd)
- Topics
- Health Sciences › Medicine › Physiology › 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
- normal brain aging, Alzheimer's disease, neuronal vulnerability, brain atrophy, neurodegeneration
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