Journal
TRENDS IN NEUROSCIENCES
Volume 39, Issue 9, Pages 625-637Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2016.07.002
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Funding
- Cure Alzheimer's Fund
- National Institute on Aging [R01 AG051521, R21-AG040683, P01-AG026572]
- Swedish Dementia Association
- Swedish Stroke Foundation
- Stone Research Foundation
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Alzheimer disease (AD) research has mainly focused on neurodegenerative processes associated with the classic neuropathologic markers of senile plaques and neurofibrillary tangles. Additionally, cerebrovascular contributions to dementia are increasingly recognized, particularly from cerebral small vessel disease (SVD). Remarkably, in AD brains, the apolipoprotein E (ApoE) epsilon 4 allele shows male excess for cerebral microbleeds (CMBs), a marker of SVD, which is opposite to the female excess of plaques and tangles. Mouse transgenic models add further complexities to sex-ApoE epsilon 4 allele interactions, with female excess of both CMBs and brain amyloid. We conclude that brain aging and AD pathogenesis cannot be understood in humans without addressing major gaps in the extent of sex differences in cerebrovascular pathology.
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