Pathological assessment of TDP-43 immunoreactive inclusions. TDP-43 immunoreactive inclusions identified in the subjects with Alzheimer disease include neuronal cytoplasmic inclusions in the dentate fascia of the hippocampus that were variable in size with some being asterisks-like and small (a), while others were larger, round, and more Pick-body like (b).

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Our cells can cut TDP-43 protein into different sized pieces, and TDP-43 protein fragments have been found in clumps from people with FTD alongside the full-size protein. Scientists think that these small fragments of TDP-43 can trigger the creation of toxic protein clumps that damage and destroy brain cells, but it is unclear how.

Arai T, Mackenzie IR, Hasegawa M, Nonoka T, Niizato K, Tsuchiya K et al ( ) Phosphorylated TDP-43 in Alzheimer's disease and dementia 

Abstract Intracellular inclusions consisting of TAR DNA binding protein-43 (TDP-43 pathology) are present in up to 57% of Alzheimer's disease (AD) cases and follow a distinct topographical pattern of progression described in the TDP-43 in AD staging scheme.

TDP-43 in Alzheimer's disease. Print; Share: Primary tabs. Details (active tab) History; Project Number. 1R01AG066729-01A1. Agency/Funding Organization. NIA. Funding Year. 2021. View Full Project Details for TDP-43 in Alzheimer's disease. Research Categorization. Primary Disease /

Transactive response DNA binding protein of 43 kDa (TDP-43) is an intranuclear protein encoded by the TARDBP gene that is involved in RNA splicing, 

Abnormal, aggregated forms of TDP-43 protein play a role in the development abnormal form of TREM2 increases the risk of developing Alzheimer's disease.

TDP-43 inclusions are found in many Alzheimer's disease (AD) patients presenting faster disease progression and greater brain atrophy.

Disorders with concomitant TDP-43 pathology (1) Alzheimer’s disease (AD) is the most frequent dementia in adults over the age of 65, presenting with loss of episodic memory, followed by impairment in other cognitive domains and behavioural changes. Pathological hallmarks of AD include neuritic plaques (extracellular deposits of β-amyloid

Several studies have indicated TDP-43 deposits in Alzheimer's disease (AD) brains and have robust connection with AD clinical phenotype. FTLD-U, which was symptomatically connected with AD, may be predictable for the comprehension of the role TDP-43 in AD. TDP-43 may contribute to AD through both β-amyloid (Aβ)-dependent and Aβ-independent