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When we think about neuropathologic changes associated with aging, the first thing that comes to mind for many of us is the development of β-amyloid plaques and tau neurofibrillary tangles which are the classic hallmarks of Alzheimer disease (AD).1 While the development of plaques and tangles often occurs in the older brain, other pathologies such as infarcts, arteriosclerosis, Lewy bodies, and TAR DNA-binding protein 43 (TDP-43) accumulation are also observed.2 TDP-43 is found in the nuclei of neurons and microglia and is involved in RNA regulation. Pathologic misfolding of this protein is seen in amyotrophic lateral sclerosis, frontotemporal dementia, AD, and limbic predominant age-related TDP-43 encephalopathy (LATE).3 Because the accumulation of abnormal proteins in the brain often leads to cognitive decline and dementia,2,4 there is a need to discover factors that play a role in the neuropathologic cascade.
Footnotes
Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.
See page 78
- Received September 6, 2022.
- Accepted in final form September 23, 2022.
- © 2022 American Academy of Neurology
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