Another is that something else causes the lesions, and the tau protein is the brain's defence against that attack.
Dr Arendt's group is now engaged in discovering exactly how the tau protein can be cleared from the brain.
One possibility is that the tau protein causes the lesions in the brain.
On emerging from hibernation, the squirrel eliminates the tau protein from its brain.
Thus, it is possible that the tau protein might not be the problem, but rather a symptom of the problem.
During hibernation, the levels of tau protein in a squirrel's hippocampal cells are directly correlated with the loss of synapses but not with the appearance of lesions.
He has conducted studies on living neurons which suggest that the tau protein is produced in response to oxidative stress, thus lending support to the protective hypothesis.
However, the Boston study showed this progressive, tau protein array in football players much too young for a dementia diagnosis, which typically occurs in people in their 70s or 80s.
He argues that the brain is armed with mechanisms for clearing the tau protein and that the reason it doesn't in people with Alzheimer's disease is because the protein is protecting the neurons.
This has led Dr Arendt to suggest that rather than being a part of a disease process, the formation of the tau protein could be a mechanism by which the brain protects itself.
The physical manifestations of the disease that Alois Alzheimer noticed in 1906 are sticky plaques of one type of protein, now known as beta-amyloid, and nerve-cell-engulfing tangles of a second type, called tau protein.
And earlier this year, a study found that when mice are subjected to stress over a period of time, they have more phosphorylated tau protein deposits in their brains (see this Scientific American blog for a nice synopsis).
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To explore the gene's role, Dr Eric Reiman and colleagues experimentally "silenced" GAB2 in neurons and observed an increase in a key protein, tau, that contributes to these tangles.
The main anatomical symptoms of Alzheimer's are the growth in the brain of plaques of a protein called beta amyloid, and tangles inside cells of a second protein called tau.
"The absence of a dose-response curve was disappointing, " says Jeffrey Cummings of UCLA. Moreover, he noted that the drug only very modestly reduced levels of a nasty protein called tau in the spinal fluid.
Another biomarker of interest is a protein called tau, implicated in the neurofibrillary tangles -- which basically take the shape of cells and destroy them -- that build up in the brains of Alzheimer's patients, particularly in the memory center called the hippocampus.
But Dr Arendt's group has made the startling discovery that hibernating brains accumulate a protein called hyperphosphorylated tau.
Peroxynitrites contribute to the hyperphosphorylation of tau proteins by oxidating g-protein coupled receptors and trysoine kinase receptors preventing protein kinase C and AKT from inactivating the enzyme GSK3 which is necessary to prevent the hyperphosphorylation of tau proteins.
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He argues that the amount of amyloid in patient brains doesn't correlate much with dementia, and blocking tau, a second protein that accumulates in the brain cells of demented patients, as his company is doing is a much better way to go.
It binds not just to tau, but also to another protein called beta amyloid, which is commonly seen in Alzheimer's disease patients.
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