Abstract

Aggregation of hyperphosphorylated tau is one of the characteristic neuropathological lesions of Alzheimer's disease and other neurodegenerative disorders. Pharmacological modulation of tau hyperphosphorylation might represent a valid and feasible therapeutic strategy for such disorders. Here, we consider recent evidence supporting the validity of the three most relevant kinases affecting tau hyperphosphorylation — GSK3, CDK5 and ERK2 — as drug targets and describe progress in the design of inhibitors for these kinases.

Author affiliations

1. Centre for Biomolecular Sciences and School of Pharmacy, University of Nottingham, University Park, Nottingham NG7 2RD, UK.

Correspondence to: Peter M. Fischer¹ Email: peter.fischer@nottingham.ac.uk

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