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Memory‐related neural systems in Alzheimer's disease: An anatomic study
Abstract
In the primate brain, there are strong connections among the entorhinal cortex, the hippocampal formation, and the amygdala, 3 structures of the ventromedial temporal lobe that are related to memory function. Because memory impairment is a central feature of Alzheimer's disease, we examined the probable cells of origin and terminal zones of these connections in the brains of humans affected by the disease, using thioflavine S, Alz-50, and anti-A4 amyloid protein immunocytochemistry. Specific cytoarchitectural areas and lamina that give rise to projections from the entorhinal cortex, the hippocampal formation, and the amygdala consistently contained neurofibrillary tangles. The terminal zones of many of these projections contained neuritic plaques, Alz-50-positive neuritic alterations, and A4 deposition. Other cytoarchitectural areas and lamina, sometimes immediately adjacent, were consistently spared from these Alzheimer changes. This pattern of Alzheimer-related alterations would disrupt projections among the entorhinal cortex, hippocampal formation, and amygdala at multiple sites, and also disrupt projections between these structures and cortical and subcortical targets. In functional terms, this pattern of structural damage is likely to be as devastating as bilateral destruction of the ventromedial temporal lobe, and thus contribute substantially to the memory disorder seen in this condition.
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“Indeed, according to Hyman et al. [29], [30], the episodic memory deficit in AD patients results from the anatomical and functional segregation of the hippocampus from associative sensory inputs due to degeneration of the perforant pathway.”
From Atrophy of presubiculum and subiculum is the earliest hippocampal anatomical marker of Alzheimer's disease (2015) · cites this paper as [29]
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Buckner, R. L., Andrews‐Hanna, J. R., & Schacter, D. L. (2008) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1440.011 · Cited by 9,761
“Several theories have offered explanations for why memory structures are particularly vulnerable to the disease, including ideas based on anatomy (Hyman et al. 1990) and also the possibility that memory structures are sensitive to toxicity because of their role in plasticity (Mesulam 2000b).”
BackgroundGauthier, S. G., Reisberg, ., Zaudig, M., Petersen, R. C., Ritchie, K. A., Broich, K., Belleville, S., Brodaty, H., Bennett, D. A., Chertkow, H. M., et al. (2006) · The Lancet · doi:10.1016/s0140-6736(06)68542-5 · Cited by 4,094
Stages in the development of Parkinson’s disease-related pathology
Braak, H., Ghebremedhin, E., Rüb, U., Bratzke, H., & Del Tredici, K. (2004) · Cell and Tissue Research · doi:10.1007/s00441-004-0956-9 · Cited by 2,689
“3B; Hyman et al. 1990; Mesulam 1998).”
Staging of alzheimer's disease-related neurofibrillary changes
Braak, H., & Braak, E. (1995) · Neurobiology of Aging · doi:10.1016/0197-4580(95)00021-6 · Cited by 2,357
Buckner, R. L., Snyder, A. Z., Shannon, B. J., LaRossa, G., Sachs, R., Fotenos, A. F., Sheline, Y. I., Klunk, W. E., Mathis, C. A., Morris, J. C., et al. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.2177-05.2005 · Cited by 2,140
“Memory networks have been described previously as having particular vulnerability in AD based on their anatomic disruption (Hyman et al., 1990) and molecular properties associated with plasticity (Mesulam, 2000).”
Background
Metadata
- Authors
- Hyman, B. T., Hoesen, G. W. V., & Damasio, A. R.
- Affiliations
- University of Iowa (US)
- ORCID
- Hyman, B. T.
- Venue
- Neurology
- Published
- 1990-11
- Volume
- 40
- Issue
- 11
- Pages
- 1721-1721
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2160683996
- Cited by
- 449
- References
- 0
- Citations by year
- 2025: 4 · 2024: 3 · 2023: 3 · 2022: 2 · 2021: 8 · 2020: 9 · 2019: 5 · 2018: 3 · 2017: 6 · 2016: 3 · 2015: 10 · 2014: 5 · 2013: 7 · 2012: 7
- FWCI
- 16.38
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG-08487)
- National Institute of Neurological Disorders and Stroke (P0 NS 19632, R01NS014944, NS-14944)
- 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 › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- Alzheimer's disease, memory impairment, entorhinal cortex, hippocampal formation, amygdala, neurofibrillary tangles, neuritic plaques, thioflavine S
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Amygdala, Brain, Hippocampus, Humans, Immunohistochemistry, Memory, Middle Aged, Neurofibrils, Temporal Lobe
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