Administration of recombinant FOXN1 protein attenuates Alzheimer's pathology in mice.

ABSTRACT:

Background

Alzheimer's disease (AD) is the most common cause of dementia in older adults and characterized by progressive loss of memory and cognitive functions that are associated with amyloid-beta (Aβ) plaques and neurofibrillary tangles. Immune cells play an important role in the clearance of Aβ deposits and neurofibrillary tangles. T cells are the major component of the immune system. The thymus is the primary organ for T cell generation. T cell development in the thymus depends on thymic epithelial cells (TECs). However, TECs undergo both qualitative and quantitative loss over time. We have previously reported that a recombinant (r) protein containing FOXN1 and a protein transduction domain can increase the number of TECs and subsequently increases the number of T cells in mic

SUBMITTER: Zhao J 

PROVIDER: S-EPMC10528256 | biostudies-literature | 2023 Oct

REPOSITORIES: biostudies-literature