Tau is implicated in a number of different forms of dementias.

A new study is looking at the earliest events associated with neurodegenerative diseases characterized by abnormal accumulation of tau protein. The research, published the prestigious journal Neuron, reveals how tau disrupts nerve-to-nerve communication at synapses and may help to guide development of therapeutic strategies that precede irreversible nerve damage.

Tau normally contributes to the supportive framework of proteins in the cell. It is meant to form the structural skeleton of the cell. It is well established that abnormal tau sometimes clumps into neuron-damaging filament deposits and that aggregates of tau with multiple phosphate groups attached are the defining feature of neurodegenerative disorders called “tauopathies”, which include Alzheimer’s disease and other dementias. Dr. Ashe and colleagues investigated how tau induces early memory deficits and disrupts communication between nerves, before actual obvious neuron damage. The researchers found that early accumulation of hyperphosphorylated tau in dendrites and dendritic spines disrupted communication coming in from other nerve cells.

Whether it’s the tau or the amyloid (a different protein) that is causing all the problems will be a focus of much research into Alzheimer’s disease and its treatment, as usual, in 2011.