Hook proteins: association with Alzheimer pathology and regulatory role of hook3 in amyloid beta generation.
Where this comes from
- Record sourced from PubMed, PMID 25799409.
- Also identified by DOI 10.1371/journal.pone.0119423 and PMC identifier 4370497.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Defects in intracellular transport are implicated in the pathogenesis of Alzheimer's disease (AD). Hook proteins are a family of cytoplasmic linker proteins that participate in endosomal transport. In this study we show that Hook1 and Hook3 are expressed in neurons while Hook2 is predominantly expressed in astrocytes. Furthermore, Hook proteins are associated with pathological hallmarks in AD; Hook1 and Hook3 are localized to tau aggregates and Hook2 to glial components within amyloid plaques. Additionally, the expression of Hook3 is reduced in AD. Modelling of Hook3 deficiency in cultured cells leads to slowing of endosomal transport and increases β-amyloid production. We propose that Hook3 plays a role in pathogenic events exacerbating AD.
Medical subject headings
- Alzheimer Disease
- Amyloid beta-Peptides
- Down-Regulation
- Microtubule-Associated Proteins