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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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Corcoran, K. A., Lu, Y., Turner, R. S., & Maren, S. (2002) · Learning & Memory · doi:10.1101/lm.51002 · Cited by 135
“The anatomy of amyloid deposition in Tg2576 mice indicates that these mice might be deficient in forms of learning that depend on the hippocampus and amygdala, for example (Hyman et al. 1990).”
BackgroundResultBarros, D. M., Izquierdo, L. A., Souza, T. M. E., Ardenghi, P. G., Pereira, P., Medina, J. H., & Izquierdo, I. (2000) · Behavioural Brain Research · doi:10.1016/s0166-4328(00)00226-6 · Cited by 132
Volumetry of amygdala and hippocampus and memory performance in Alzheimer's disease
Basso, M. R., Yang, J., Warren, L. H., MacAvoy, M. G., Varma, P., Bronen, R. A., & van Dyck, C. H. (2006) · Psychiatry Research Neuroimaging · doi:10.1016/j.pscychresns.2006.01.007 · Cited by 137
“Although these findings occur in a range of brain structures, the site of earliest and most severe pathology in AD is the medial temporal lobe (Hyman et al., 1990; Braak and Braak, 1991).”
BackgroundWorking memory and apolipoprotein E: What's the connection?
Rosen, V. M. (2002) · Neuropsychologia · doi:10.1016/s0028-3932(02)00132-x · Cited by 131
Ginsberg, S. D., Mufson, E. J., Counts, S., Wuu, J., Alldred, M. J., Nixon, R. A., & Che, S. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-101080 · Cited by 134
Evolution of Alzheimer’s disease related cortical lesions
Braak, H., Braak, E., Bohl, J. R. E., & Bratzke, H. (1998) · Journal of neural transmission. Supplementum · doi:10.1007/978-3-7091-7508-8_9 · Cited by 127
Changes in Plasticity Across the Lifespan
Oberman, L. M., & Pascual‐Leone, Á. (2013) · Progress in brain research · doi:10.1016/b978-0-444-63327-9.00016-3 · Cited by 134
“The reason why memory structures are particularly vulnerable to AD and critically involved in disease progression remains unclear, though proposed theories include concepts based on anatomy (Hyman et al., 1990) and on mechanisms of plasticity (Mesulam, 2000).”
BackgroundPropagation of tau pathology in Alzheimer’s disease: identification of novel therapeutic targets
Pooler, A. M., Polydoro, M., Wegmann, S., Nicholls, S. B., Spires‐Jones, T. L., & Hyman, B. T. (2013) · Alzheimer s Research & Therapy · doi:10.1186/alzrt214 · Cited by 130
“The loss of NFT-affected neurons results in disconnection and deafferentation of critical neural circuits [8] and thus is likely to contribute to the defects in memory and higher-order cognitive functions in AD.”
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Assessing neuronal networks: Understanding Alzheimer's disease
Bokde, A. L. W., Ewers, M., & Hampel, H. J. (2009) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2009.06.004 · Cited by 120
“It has been found that the projections among the hippocampal formation, entorhinal cortex, and amygdala contained NFT and the ends of the projections contained amyloid deposition (Hyman et al., 1990).”
BackgroundLife and Death of Neurons in The Aging Cerebral Cortex
Morrison, J. H., & Hof, P. R. (2007) · International review of neurobiology · doi:10.1016/s0074-7742(06)81004-4 · Cited by 120
Brain sites involved in fear memory reconsolidation and extinction of rodents
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Hof, P. R. (1992) · Archives of Neurology · doi:10.1001/archneur.1992.00530330070019 · Cited by 118
Cognitive correlates of alterations in acetylcholinesterase in Alzheimer's disease
Bohnen, N. I., Kaufer, D., Hendrickson, R., Ivanco, L. S., Lopresti, B. J., Davis, J. G., Constantine, G. M., Mathis, C. A., Moore, R. Y., & DeKosky, S. T. (2005) · Neuroscience Letters · doi:10.1016/j.neulet.2005.01.031 · Cited by 116
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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