Abstract:
:The deposition of amyloid-β (Aβ) plaques and tau-based neurofibrillary tangles is a neuropathological feature of Alzheimer's disease (AD). While studies have shown that the Aβ and tau interaction results in elevated AD pathology, the molecular linkage and mechanism of interaction of Aβ and tau are unclear. A recent study demonstrated the direct interaction between the Aβ core and specific regions of tau that facilitates pathological cross-seeding via a shared epitope. The data suggest that targeting the common epitope could be a more effective treatment strategy rather than targeting only Aβ or only tau. The findings have an important clinical significance for AD and related tauopathies.
journal_name
Biochemistryjournal_title
Biochemistryauthors
Tripathi T,Khan Hdoi
10.1021/acs.biochem.9b01087subject
Has Abstractpub_date
2020-02-04 00:00:00pages
341-342issue
4eissn
0006-2960issn
1520-4995journal_volume
59pub_type
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