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Arthur T Knackerbracket has found the following story:
Researchers at the German Center for Neurodegenerative Diseases (DZNE) and the Institute for Stroke and Dementia Research (ISD) at the University Hospital of the Ludwig-Maximilians-Universität (LMU) in Munich have found that a protein called TREM2 could positively influence the course of Alzheimer's disease. When TREM2 is present in the cerebrospinal fluid at higher concentrations, patients at any stage of the disease have a better prognosis. This observation provides a starting point for the development of new therapeutic strategies. The study was led by Prof. Christian Haass (DZNE) and Prof. Michael Ewers (ISD, LMU) and is published in the journal “Science Translational Medicine”.
[...] In previous studies on mice, Haass and his colleagues demonstrated that TREM2 activates microglia to enclose and selectively destroy toxic protein aggregates typical for Alzheimer’s disease. “These observations indicate that TREM2 can protect the brain from the degenerative effects of the disease – at least in animal models,” said Haass.
[...using] data of 385 subjects from the Alzheimer's Disease Neuroimaging Initiative (ADNI), a large clinical dataset containing records and samples from patients and healthy seniors taken at regular checkups over many years. The study thus allows to establish associations between certain biochemical changes and disease progression.
Indeed, Haass and Ewers found that high levels of TREM2 improved the prognosis of subjects at all stages of the disease. Their memory remained more stable and the degradation of the hippocampus, a brain region responsible for learning and recollection, was less pronounced.
“Our findings are clinically relevant because we found that higher levels of TREM2 were associated also with a reduced rate of the development of full blown dementia over a time period up to 11 years”, explained Ewers. “Microglia activation is a double-edged sword, entailing both protective effects and neurotoxic inflammation. TREM2 signaling may play a key role in the regulation of the brain’s protective immune response”.
Increased soluble TREM2 in cerebrospinal fluid is associated with reduced cognitive and clinical decline in Alzheimer’s disease; Michael Ewers, Nicolai Franzmeier, Marc Suárez-Calvet et al.; Science Translational Medicine (2019); DOI: 10.1126/scitranslmed.aav6221
(Score: 2) by Ken_g6 on Saturday August 31 2019, @05:19AM (2 children)
I read that as "this may treat Alzheimer's but it may kill you in the end." Still a potentially useful tradeoff. I wonder what the chances are that this will cause Parkinson's [soylentnews.org] instead?
I tend to think a cure will come by preventing bacteria from getting to the brain [soylentnews.org] in the first place, so the immune system doesn't have to contain them with protein aggregates or mop them up with microglia. Perhaps preventing hardening of the arteries [cam.ac.uk] would help?
(Score: 2) by takyon on Saturday August 31 2019, @05:24AM
Nanobots with lasers.
[SIG] 10/28/2017: Soylent Upgrade v14 [soylentnews.org]
(Score: 1) by ze on Saturday August 31 2019, @05:25PM
Like any immune response, inflammation is bad, except when and where you need it. That double-edge is standard for lots of maintenance processes.
The way I read this is just that the microglia activation is only helpful where it's needed, and this TREM2 stuff seems to regulate its activation, so this sounds like an overall helpful discovery, and not a treatment that'll kill you.