The tangled biology of tau.

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With the aging of the population comes a heightened sense of urgency to do something about Alzheimer’s disease (AD), the most common dementia disorder. Treatment for AD is essentially nonexistent, but progress in understanding its molecular basis is encouraging. Recently, studies on the etiology of AD focused on the pathogenesis of two pathognomonic features, senile plaques and neurofibrillary tangles. First seen almost a century ago by Alois Alzheimer (1), these plaques and tangles are composed principally of the proteins Aβ (2) and tau (3), respectively. Identification of Aβ mutations in patients with AD argues that Aβ plays an important role in AD pathogenesis (4). But the role of tau in neurodegeneration was less certain until recent discoveries that mutations in the tau gene can cause non-Alzheimer’s dementia (5–9).