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Regional distribution of synaptic markers and APP correlate with distinct clinicopathological features in sporadic and familial Alzheimer’s disease
Open accessAbstract
Recent studies suggest that subcortical structures, including striatum, are vulnerable to amyloid-β accumulation and other neuropathological features in familial Alzheimer's disease due to autosomal dominant mutations. We explored differences between familial and sporadic Alzheimer's disease that might shed light on their respective pathogenic mechanisms. To this end, we analysed 12 brain regions, including neocortical, limbic and subcortical areas, from post-mortem brains of familial Alzheimer's disease (n = 10; age at death: 50.0 ± 8.6 years) with mutations in amyloid precursor protein (APP) or presenilin 1 (PSEN1), sporadic Alzheimer's disease (n = 19; age at death: 84.7 ± 7.8 years), neurologically normal elderly without amyloid-β accumulation (normal ageing; n = 13, age at death: 82.9 ± 10.8 years) and neurologically normal elderly with extensive cortical amyloid-β deposits (pathological ageing; n = 15; age at death: 92.7 ± 5.9 years). The levels of amyloid-β₄₀, amyloid-β₄₂, APP, apolipoprotein E, the synaptic marker PSD95 (now known as DLG4), the astrocyte marker GFAP, other molecules related to amyloid-β metabolism, and tau were determined by enzyme-linked immunosorbent assays. We observed that familial Alzheimer's disease had disproportionate amyloid-β₄₂ accumulation in subcortical areas compared with sporadic Alzheimer's disease, whereas sporadic Alzheimer's disease had disproportionate amyloid-β₄₂ accumulation in cortical areas compared to familial Alzheimer's disease. Compared with normal ageing, the levels of several proteins involved in amyloid-β metabolism were significantly altered in both sporadic and familial Alzheimer's disease; however, such changes were not present in pathological ageing. Among molecules related to amyloid-β metabolism, the regional distribution of PSD95 strongly correlated with the regional pattern of amyloid-β₄₂ accumulation in sporadic Alzheimer's disease and pathological ageing, whereas the regional distribution of APP as well as β-C-terminal fragment of APP were strongly associated with the regional pattern of amyloid-β₄₂ accumulation in familial Alzheimer's disease. Apolipoprotein E and GFAP showed negative regional association with amyloid-β (especially amyloid-β₄₀) accumulation in both sporadic and familial Alzheimer's disease. Familial Alzheimer's disease had greater striatal tau pathology than sporadic Alzheimer's disease. In a retrospective medical record review, atypical signs and symptoms were more frequent in familial Alzheimer's disease compared with sporadic Alzheimer's disease. These results suggest that disproportionate amyloid-β₄₂ accumulation in cortical areas in sporadic Alzheimer's disease may be mediated by synaptic processes, whereas disproportionate amyloid-β₄₂ accumulation in subcortical areas in familial Alzheimer's disease may be driven by APP and its processing. Region-specific amyloid-β₄₂ accumulation might account for differences in the relative amounts of tau pathology and clinical symptoms in familial and sporadic Alzheimer's disease.
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“Positive regional associations between LRP1 and insoluble Aβ42 levels have also been detected in individuals without dementia (12) and in familial AD cases (13).”
From APOE4-mediated amyloid-β pathology depends on its neuronal receptor LRP1 (2019) · cites this paper as [13]
In the citing paper
“Currently it is known that the distribution of Aβ and tau accumulation is different in FAD and sAD, with more present in subcortical regions in FAD [147].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [147]
In the citing paper
“and atypical cognitive symptoms are more likely to be present in FAD [147].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [147]
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Metadata
- Authors
- Shinohara, M., Fujioka, S., Murray, M. E., Wojtas, A., Baker, M., Rovelet-Lecrux, A., Rademakers, R., Das, P., Parisi, J. E., Graff-Radford, N. R., Petersen, R. C., Dickson, D. W., & Bu, G.
- Affiliations
- Mayo Clinic in Florida (US)
- Mayo Clinic (US)
- ORCID
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-03-12
- Volume
- 137
- Issue
- 5
- Pages
- 1533-1549
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC3999719
- OpenAlex
- W2073744343
- Cited by
- 115
- References
- 63
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 6 · 2023: 9 · 2022: 2 · 2021: 12 · 2020: 11 · 2019: 17 · 2018: 10 · 2017: 9 · 2016: 19 · 2015: 8 · 2014: 3
- FWCI
- 8.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Funders
- Mayo Clinic
- Alzheimer's Drug Discovery Foundation
- Naito Foundation
- Japan Heart Foundation
- National Institutes of Health
- National Institute on Aging (P01AG030128, P01 AG030128-PROJECT 3, R01AG027924, U01AG006786, RF1AG046205, R01AG035355, P50AG016574)
- National Institute of Neurological Disorders and Stroke (P01 NS074969-PROJECT 3, P01NS074969)
- 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, familial Alzheimer's disease, sporadic Alzheimer's disease, amyloid-beta 42, Aβ40, amyloid precursor protein, presenilin 1, PSD-95, synaptic markers, apolipoprotein E, glial fibrillary acidic protein, amyloid-beta metabolism, pathological aging, regional distribution
- MeSH terms
- Adult, Aged, Aged, 80 and over, Alzheimer Disease, Brain, Female, Humans, Male, Middle Aged, Nerve Tissue Proteins, Postmortem Changes, Synapses, Amyloid beta-Peptides, Aspartic Acid Endopeptidases, Amyloid beta-Protein Precursor, Neurofibrillary Tangles, tau Proteins, Presenilin-1, Amyloid Precursor Protein Secretases
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