Then, the researchers seeded the mice's brains with small amounts of tau collected from Alzheimer's patients.

It appears tau is routinely released during waking hours by brain activity and then decreases during sleep, allowing tau to be cleared away.

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The study included up to 4 years of data on cognition and amyloid PET imaging, and up to 3 years of tau PET imaging data.

As a pathological hallmark of AD, NFTs are intracellular inclusions composed of hyper-p-tau arranged in paired helical filaments (PHFs).[20],[21] Although the role of p-tau in AD pathology is thought to be secondary to A[sz] accumulation in the brain, a growing body of evidence suggests that tau has unique roles in AD that are A[sz] independent.

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Pretangle tau emerges in the LC in individuals around 40 years old, yet degeneration of LC neurons is not apparent until mid-stage AD, suggesting that LC neurons could be harboring pathogenic tau species throughout the decades-long prodromal stage of AD.

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Mouse monoclonal and rabbit affinity purified polyclonal anti-tau antibodies were both raised against a 166-AA tau fragment containing the central region of the protein that is shared among tau isoforms.

In many forms of dementia, such as Alzheimer's disease and chronic traumatic encephalopathy caused by multiple concussions, the tau protein starts behaving badly and instead of performing its normal cellular functions, it begins accumulating and interfering with cell-to-cell communications.

“We are very pleased to welcome Kerstin Berns and her team of consultants to join the TAUS representatives,” says Jaap van der Meer, director of TAUS.