Journal
ACTA NEUROPATHOLOGICA COMMUNICATIONS
Volume 6, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s40478-018-0641-y
Keywords
FTD; VCID; Arteriosclerosis; Apolipoprotein E
Categories
Funding
- NIH from the National Institute on Aging (NIA)/National Institutes of Health (NIH) [P30 AG028383, R01 AG057187, R01 AG042475, R01 AG054060, U01 AG016976]
- NIA/NIH [U01 AG016976]
- NIA [P30 AG019610, P30 AG013846, P50 AG008702, P50 AG025688, P50 AG047266, P30 AG010133, P50 AG005146, P50 AG005134, P50 AG016574, P50 AG005138, P30 AG008051]
- [P30 AG013854]
- [P30 AG008017]
- [P30 AG010161]
- [P50 AG047366]
- [P30 AG010129]
- [P50 AG016573]
- [P30 AG053760]
- [P30 AG010124]
- [P50 AG005133]
- [P50 AG005142]
- [P50 AG005131]
- [P50 AG023501]
- [P30 AG035982]
- [P30 AG012300]
- [P30 AG049638]
- [P50 AG005136]
- [P50 AG033514]
- [P50 AG005681]
- [P50 AG047270]
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TAR-DNA binding protein 43 (TDP-43) proteinopathy is a common brain pathology in elderly persons, but much remains to be learned about this high-morbidity condition. Published stage-based systems for operationalizing disease severity rely on the involvement (presence/absence) of pathology in specific anatomic regions. To examine the comorbidities associated with TDP-43 pathology in aged individuals, we studied data from the National Alzheimer's Coordinating Center (NACC) Neuropathology Data Set. Data were analyzed from 929 included subjects with available TDP-43 pathology information, sourced from 27 different American Alzheimer's Disease Centers (ADCs). Cases with relatively unusual diseases including autopsy-proven frontotemporal lobar degeneration (FTLD-TDP or FTLD-tau) were excluded from the study. Our data provide new information about pathologic features that are and are not associated with TDP-43 pathologies in different brain areasspinal cord, amygdala, hippocampus, entorhinal cortex/inferior temporal cortex, and frontal neocortex. Different research centers used cite-specific methods including different TDP-43 antibodies. TDP-43 pathology in at least one brain region was common (31.4%) but the pathology was rarely observed in spinal cord (1.8%) and also unusual in frontal cortex (5.3%). As expected, TDP-43 pathology was positively associated with comorbid hippocampal sclerosis pathology and with severe AD pathology. TDP-43 pathology was also associated with comorbid moderate-to-severe brain arteriolosclerosis. The association between TDP-43 pathology and brain arteriolosclerosis appears relatively specific since there was no detected association between TDP-43 pathology and microinfarcts, lacunar infarcts, large infarcts, cerebral amyloid angiopathy (CAA), or circle of Willis atherosclerosis. Together, these observations provide support for the hypothesis that many aged brains are affected by a TDP-43 proteinopathy that is more likely to be seen in brains with AD pathology, arteriolosclerosis pathology, or both.
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