Tau in Alzheimer’s Disease: Pathological Alterations and an Attractive Therapeutic Target

Jan 11, 2021Current medical science

Changes in Tau Protein in Alzheimer's Disease and Its Potential as a Treatment Target

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Abstract

The number of neurofibrillary tangles correlates positively with the severity of dementia in Alzheimer's disease.

Alzheimer's disease is characterized by the presence of amyloid plaques and neurofibrillary tangles.
Neurofibrillary tangles consist of abnormally hyperphosphorylated tau protein.
The prion-like seeding and spreading of tau pathology may drive the progression of Alzheimer's disease.
Abnormal tau hyperphosphorylation contributes to neurodegeneration in various neurodegenerative disorders.
Recent research has identified tau protein as a potential target for therapeutic interventions in Alzheimer's disease.

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Alzheimer's disease (AD) is an age-related neurodegenerative disease with two major hallmarks: extracellular amyloid plaques made of amyloid-β (Aβ) and intracellular neurofibrillary tangles (NFTs) of abnormally hyperphosphorylated tau. The number of NFTs correlates positively with the severity of dementia in AD patients. However, there is still no efficient therapy available for AD treatment and prevention so far. A deeper understanding of AD pathogenesis has identified novel strategies for the generation of specific therapies over the past few decades. Several studies have suggested that the prion-like seeding and spreading of tau pathology in the brain may be a key driver of AD. Tau protein is considered as a promising candidate target for the development of therapeutic interventions due to its considerable pathological role in a variety of neurodegenerative disorders. Abnormal tau hyperphosphorylation plays a detrimental pathological role, eventually leading to neurodegeneration. In the present review, we describe the recent research progresses in the pathological mechanisms of tau protein in AD and briefly discuss tau-based therapeutic strategies.

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Tau in Alzheimer’s Disease: Pathological Alterations and an Attractive Therapeutic Target

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