A Surprising New Weapon Against Alzheimer’s

One of the putative causal factors potentially mediating Alzheimer’s pathogenesis is the aggregation of tau proteins in the brain.

Translated from sciencese: tau proteins getting stuck in the brain may be at least partly responsible for Alzheimer’s disease.

So, what to do about it?

Get tau’t of the way

Researchers (Dr. Sofia Bali et al.) may have a novel solution: replace sticky tau proteins with modified tau proteins that are able to slip-and-slide as necessary, while still doing the job they’re supposed to (because yes, there are supposed to be tau proteins in the brain; they’re just not supposed to clump together and get stuck).

You may be wondering what tau’s job is supposed to be: tau stabilizes microtubules, which act as intracellular transport highways for vesicles, organelles, and other cellular components. This is important, because loss of this function contributes to neurodegenerative disease just as badly as toxic aggregation of tau does.

Diseases that come about as a result of tau dysfunction (in one way or another) or called tauopathies. Most tauopathies, including Alzheimer’s disease, frontotemporal dementia, chronic traumatic encephalopathy, and progressive supranuclear palsy, are driven primarily by aggregation of the 4R isoform of tau, but preventing this without disrupting the microtubule binding that we talked about has been a major challenge, to say the least.

So, Dr. Bali and her team altered some of the amino acids in the region that normally the potentially pathogenic 4R isoform to an amyloid-forming motif, borrowing sequence features from the non-pathogenic 3R isoform.

That might be hard to visualize, so think of it this way: these substitutions caused the modified tau fragments to fold into a rigid, hairpin-like shape, physically blocking interactions and preventing clump formation.

Does it work? Per the team’s experimentations… Yes, it works, in vitro at least. Whether it works in a living human brain has yet to be tested, and doubtlessly non-human animal tests will be done first.

You can find the paper itself, here: Amyloid-motif-dependent tau self-assembly is modulated by isoform sequence context

What to do about it meanwhile?

Since that won’t be hitting the prescription pads for a while yet, it’s worth staying ahead of the game with such strategies as:

• Alzheimer’s Causative Factors To Avoid
• How To Reduce Your Alzheimer’s Risk

And to get those tau proteins moving like they should, you might consider:

Spermine vs Alzheimer’s & Parkinson’s!

And if you’re wondering to what extent you’re at risk, then do check out:

• Early Dementia Screening From Your Blood & More
• How To Actually Access Early Dementia Screening

Want to learn more?

For a much more in-depth coverage of the topic of Alzheimer’s treatment on the level of the personal rather than the molecular, you might like this excellent book we reviewed a while back:

The Spectrum of Hope: An Optimistic and New Approach to Alzheimer’s Disease and Other Dementias – by Dr. Gayatri Devi

Take care!