Glymphatic inhibition exacerbates tau propagation in an Alzheimer's disease model.

ABSTRACT:

Background

The aggregation and spread of misfolded amyloid structured proteins, such as tau and α-synuclein, are key pathological features associated with neurodegenerative disorders, including Alzheimer's and Parkinson's disease. These proteins possess a prion-like property, enabling their transmission from cell to cell leading to propagation throughout the central and peripheral nervous systems. While the mechanisms underlying their intracellular spread are still being elucidated, targeting the extracellular space has emerged as a potential therapeutic approach. The glymphatic system, a brain-wide pathway responsible for clearing extracellular metabolic waste from the central nervous system, has gained attention as a promising target for removing these toxic proteins.

Methods<

SUBMITTER: Lopes DM 

PROVIDER: S-EPMC10996277 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature