Tau aggregation is a therapeutic target for Alzheimer's disease.

Abstract:

:Based on the amyloid hypothesis, studies for AD therapy have been mostly focused on removing β-amyloid. Recent results of amyloid immunotherapy raised the question whether β-amyloid is sufficient target for AD therapy. Neurofibrillary tangles (NFTs), which contain hyperphosphorylated tau, are another pathological hallmark of AD. NFTs are observed in entorhinal cortex, limbic, and neocortex over the course of clinical progression. NFTs are associated with synapse and neuron loss, suggesting that the process of NFT formation is involved in brain dysfunction. During NFT formation, tau forms a variety of different aggregation species, including tau oligomers, granules, and fibrils. Analysis of different human tau-expressing mouse lines reveals that soluble hyperphosphorylated tau, which includes tau oligomer, is involved in synapse loss, whereas granular tau formation is involved in neuronal loss. Therefore, inhibition of tau aggregation and tau phosphorylation is expected to prevent synapse loss and neuron loss, and may slow or halt the progressive dementia in AD.

journal_name

Curr Alzheimer Res

authors

Takashima A

doi

10.2174/156720510793611600

subject

Has Abstract

pub_date

2010-12-01 00:00:00

pages

665-9

issue

8

eissn

1567-2050

issn

1875-5828

pii

CAR -88

journal_volume

7

pub_type

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