Alzheimer's-type neuropathology in the precuneus is not increased relative to other areas of neocortex across a range of cognitive impairment
Open accessAbstract
We studied Alzheimer's disease (AD) pathology in the precuneus and surrounding brain areas. Anatomically, the precuneus corresponds to the medial portion of human cerebral cortical Brodmann Area 7. This study utilized patients from the University of Kentucky Alzheimer's Disease Center autopsy cohort. Data from 47 brains were used comprising patients of differing antemortem cognitive impairment severities, each with longitudinal clinical data and extensive neuropathological data. We assessed whether the precuneus and surrounding areas are differentially vulnerable to AD-type pathological lesions (diffuse amyloid plaques, neuritic amyloid plaques, and neurofibrillary tangles). Eleven areas of brain were evaluated for each case: amygdala, hippocampal CA1, subiculum, entorhinal cortex, frontal cortex, superior and middle temporal gyri, inferior parietal lobule, occipital cortex, posterior cingulate gyrus, Brodmann Area 31, and the precuneus proper. Like other areas of neocortex, the precuneus demonstrated increased diffuse and neuritic amyloid plaques early in the evolution in AD, and increased neurofibrillary tangles late in AD. Correcting for the antemortem cognitive status of the patients, there was no evidence of an increase in the density of AD-type pathology in the precuneus or neighboring areas relative to other areas of cerebral neocortex. Our results are not consistent with the idea that the precuneus is involved in a special way with plaques or tangles relative to other areas of neocortex.
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Evaluation of AD status was conducted using National Institute on Aging Reagan Institute guidelines including evaluation of neurofibrillary tangles and neuritic senile plaques.
“Evaluation of AD status was conducted by the AD Center Neuropathology and Clinical Cores using guidelines set forth by the National Institute on Aging Reagan Institute that included evaluation of neurofibrillary tangles and neuritic senile plaques [36–38].”
From Predominant expression of Alzheimer’s disease-associated BIN1 in mature oligodendrocytes and localization to white matter tracts (2016) · cites this paper as [36]
The study description (page unavailable) says the University of Kentucky Alzheimer’s Disease Center routinely counted neurofibrillary tangles and neuritic plaques, and that patients received post-mortem consensus diagnoses. Our copy does not state that AD status was evaluated under National Institute on Aging–Reagan Institute guidelines or identify the AD Center Neuropathology and Clinical Cores as conducting that evaluation. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPIB retention within a brain generally indicates the presence of Aβ plaques.
“Brain retention may reflect plaque or non-plaque fibrillar Aβ binding, and possibly also Aβ-independent phenomena, but PIB retention within a brain generally indicates the presence of Aβ plaques [69, 70].”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [70]
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- Authors
- Nelson, P. T., Abner, E. L., Scheff, S. W., Schmitt, F. A., Kryscio, R. J., Jicha, G. A., Smith, C. D., Patel, E., & Markesbery, W. R.
- Affiliations
- University of Kentucky (US)
- Corresponding author
- Nelson, Peter T.
- ORCID
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 2009-02
- Volume
- 450
- Issue
- 3
- Pages
- 336-339
- ISSN
- 0304-3940 (ISSN-L)
- PMC
- PMC2839166
- OpenAlex
- W2162755825
- Cited by
- 70
- References
- 27
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 3 · 2022: 5 · 2021: 4 · 2020: 2 · 2019: 2 · 2018: 4 · 2017: 6 · 2016: 3 · 2015: 1 · 2014: 6 · 2013: 7 · 2012: 9
- FWCI
- 3.39
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (P50AG005144, P30AG028383)
- National Institute of Neurological Disorders and Stroke (K08NS050110)
- 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 › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, precuneus, amyloid plaques, neurofibrillary tangles, cognitive impairment, neocortex, posterior cingulate cortex
- MeSH terms
- Aged, 80 and over, Alzheimer Disease, Amygdala, Brain Mapping, Cognition Disorders, Hippocampus, Humans, Nerve Degeneration, Neurons, Parietal Lobe, Neurofibrillary Tangles, Disease Progression, Neocortex, Plaque, Amyloid
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