Absence of tissue transglutaminase reduces amyloid-beta pathology in APP23 mice.

ABSTRACT:

Aims

Alzheimer's disease (AD) is characterised by amyloid-beta (Aβ) aggregates in the brain. Targeting Aβ aggregates is a major approach for AD therapies, although attempts have had little to no success so far. A novel treatment option is to focus on blocking the actual formation of Aβ multimers. The enzyme tissue transglutaminase (TG2) is abundantly expressed in the human brain and plays a key role in post-translational modifications in Aβ resulting in covalently cross-linked, stable and neurotoxic Aβ oligomers. In vivo absence of TG2 in the APP23 mouse model may provide evidence that TG2 plays a key role in development and/or progression of Aβ-related pathology.

Methods

Here, we compared the effects on Aβ pathology in the presence or absence of TG2 using 12-month-old wild

SUBMITTER: Wilhelmus MMM 

PROVIDER: S-EPMC9304226 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature