Synaptic proteins, neuropathology and cognitive status in the oldest-old
Open accessAbstract
An increasing number of individuals in our population are surviving to over 90 years and a subset is at risk for developing dementia. However, senile plaque and neurofibrillary tangle pathology do not consistently differentiate individuals with and without dementia. Synaptic protein loss is a feature of aging and dementia and may dissociate 90+ individuals with and without dementia. Synaptophysin (SYN), postsynaptic density 95 (PSD-95) and growth-associated protein 43 (GAP-43) were studied in the frontal cortex of an autopsy series of 32 prospectively followed individuals (92-105 years) with a range of cognitive function. SYN protein levels were decreased in individuals with dementia and increased in those with clinical signs of cognitive impairment insufficient for a diagnosis of dementia. SYN but neither PSD-95 nor GAP-43 protein levels were significantly correlated with mini-mental status examination (MMSE) scores. Frontal cortex SYN protein levels may protect neuronal function in oldest-old individuals and reflect compensatory responses that may be involved with maintaining cognition.
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A sizable percentage of non-demented elderly have plaques.
“Decades of clinical-pathological correlative studies, now corroborated by a decade of neuroimaging studies, also demonstrate a sizable percentage of the non-demented elderly have plaques [40, 51, 54, 55, 58–68].”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [59]
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- Authors
- Head, E., Corrada, M. M., Kahle-Wrobleski, K., Kim, R. C., Sarsoza, F., Goodus, M., & Kawas, C. H.
- Affiliations
- University of California, Irvine (US)
- Corresponding author
- Head, Elizabeth
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2009-07
- Volume
- 30
- Issue
- 7
- Pages
- 1125-1134
- ISSN
- 0197-4580 (ISSN-L)
- PMC
- PMC7295175
- OpenAlex
- W2105762907
- Cited by
- 145
- References
- 58
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 21 · 2023: 11 · 2022: 7 · 2021: 4 · 2020: 16 · 2019: 6 · 2018: 8 · 2017: 7 · 2015: 3 · 2014: 6 · 2013: 5 · 2012: 5
- FWCI
- 4.14
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- American Academy of Neurology
- National Institutes of Health
- National Institute on Aging (R01AG021055, Z01AG000658, P50AG016573, P50 AG000658)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- synaptic proteins, synaptophysin, PSD-95, GAP-43, oldest old, dementia, cognitive impairment, frontal cortex, compensatory mechanisms, cognitive aging, neuropathology
- MeSH terms
- Disks Large Homolog 4 Protein, Aged, 80 and over, Aging, Cognition Disorders, Dementia, Female, Frontal Lobe, Humans, Male, Membrane Proteins, Neuropsychological Tests, Prospective Studies, Synaptic Membranes, Cohort Studies, Biomarkers, Synaptophysin, Disease Progression, GAP-43 Protein, Intracellular Signaling Peptides and Proteins
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