The effect of age and Alzheimer's disease on pyramidal neuron density in the individual fields of the hippocampal formation
Abstract
Pyramidal neuron density was determined at autopsy in the brains of 12 neurologically normal patients (age range 6-87 years) and 18 patients with histopathologically confirmed Alzheimer's disease (AD; age range 62-89 years). Paraffin wax sections were cut at the level of the central part of the cornu ammonis and stained with cresyl fast violet. Pyramidal neuron density was determined in the stratum pyramidale of the presubiculum, subiculum, prosubiculum and CA1-4. The width of the stratum pyramidale in these areas was also determined. There was no significant effect of age on pyramidal neuron density in any of the fields of the hippocampal formation. However, there was a significant decrease in pyramidal neuron density in the subiculum (44%), prosubiculum (28%) and CA1 (41%) of AD brains compared to controls. There was no significant effect of AD on pyramidal neuron density in the presubiculum, CA2 and CA3, but in CA4 it increased (23%) significantly. Pyramidal band width decreased significantly with age in the presubiculum but there was no effect of age on any other region of the hippocampal formation investigated. The width of the stratum pyramidale was significantly lower in the presubiculum (19%), subiculum (30%) and CA3 (17%) of AD compared with control brains. These data suggest that a reduction in pyramidal neuron density within the hippocampal formation does not occur in the absence of underlying pathology. In AD, pyramidal neuron loss predominantly occurs from that sector of the hippocampal formation which comprises the subiculum, prosubiculum and CA1.
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The CA1 region is one of the earliest and more affected brain regions in AD patients.
“In contrast to 5xFAD, other FAD mouse models show clear intraneuronal Aβ accumulation and neuronal loss in the CA1 region [7, 16, 88], which has also been shown to be one of the earliest and more affected brain regions in AD patients [4, 27, 68, 82].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [27]
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References 41 · Cited by 88
- Authors
- Davies, D. C., Horwood, N., Isaacs, S. L., & Mann, D. M. A.
- Affiliations
- St George's, University of London (GB)
- St Mary's Hospital (GB)
- University of Manchester (GB)
- Venue
- Acta Neuropathologica
- Published
- 1992-04
- Volume
- 83
- Issue
- 5
- Pages
- 510-517
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- OpenAlex
- W2073227535
- Cited by
- 88
- References
- 41
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 4 · 2020: 4 · 2019: 4 · 2016: 3 · 2015: 4 · 2014: 4 · 2013: 4 · 2012: 1
- FWCI
- 3.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Acta Neuropathologica (publishedVersion)
- PubMed (publishedVersion)
- 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 › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- Alzheimer's disease, pyramidal neurons, neuronal density, hippocampal formation, cornu ammonis, subiculum, presubiculum, CA1, CA4, age effects, neuronal loss, neuropathology
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Aging, Alzheimer Disease, Child, Female, Hippocampus, Humans, Male, Middle Aged, Neurons, Pyramidal Tracts, Paraffin Embedding
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