About half of all individuals with AD (Alzheimer's disease) dementia have TDP-43 proteinopathy as an additional co-pathology. TDP-43 proteinopathy is primarily intraneuronal accumulations of phosphorylated TDP-43. The accumulation pattern of TDP-43 has recently been described as LATE-NC (limbic age-associated TDP-43 encephalopathy neuropathological change). To better understand the role of LATE-NC in AD dementia, we asked the following:

1) When in the clinical course of AD does LATE-NC appear?

2) When in the development of AD pathology does LATE-NC appear?

3) Is LATE-NC purely age-associated?

4) Besides prevalence, is LATE-NC severity also important?

We designed a clinicopathological study using 522 individuals in the CNDR (Center for Neurodegenerative Disease Research) cohort to assess the clinical significance of LATE-NC in AD dementia. 

*Note: This poster extracts findings and data from an unpublished study on co-pathologies in Alzheimer's disease. This presentation highlights LATE-NC. Co-pathologies not addressed in this presentation include cerebral amyloid angiopathy (CAA) and Lewy bodies. Other AD-related pathologies include aging-related tau astrogliopathy, ischaemic injury, and other non-CAA vascular pathologies. Findings from the CNDR cohort were compared with a larger cohort of 1,340 participants in the National Alzheimer Coordinating Center database.