Four new studies call into question PLD3’s status as an AD risk factor. Larger studies may be needed to settle the debate.
The Centers for Medicare and Medicaid services has given the nod to an 18,000-patient study to see whether amyloid scans prove their worth. Researchers hope for coverage afterward.
Senataxin, a gene associated with early onset ALS, regulates how cells respond to viruses.
Researchers link the AD Risk gene BIN1 to tau and amyloid in different model systems, and propose a mechanism for how a PICALM variant might be protective.
Scientists have found that the nuclear receptor ERRγ ramps up mitochondrial energy production in neurons.
Researchers no longer debate whether misfolded proteins spread through the brain in neurodegenerative disease. Now they want to know how.
Blamed for neurodegeneration and memory problems, the transcription factor ATF4 may also be a gatekeeper for synaptic plasticity and memory formation.
The same or similar molecules might treat a variety of protein-misfolding conditions.
Ever since amyloid PET tracers started getting approved for clinical use in 2012, clinicians have wanted to use them widely to clarify uncertain diagnoses. When the Centers for Medicare & Medicaid Services declined coverage without more evidence showing that scans improve patient outcomes, scientists designed a national study, which the agency has now approved and agreed to fund. Called Imaging Dementia—Evidence for Amyloid Scanning (IDEAS for short), the $100 million study will pay for scans for almost 18,500 patients and assess whether the scans changed their diagnoses or treatment, or helped prevent subsequent health emergencies.
Four new studies in Nature call into the question the status of phospholipase D3, a protein previously linked to Alzheimer’s disease through genetic studies. An original report had identified three variants in the gene that increased the chances of getting AD up to twofold. Now, studies conducted in different European cohorts report no association between two of those variants and AD, and only a weak association with the third. They conclude it’s unlikely that PDL3 is an AD risk gene. Only data from larger sequencing projects will be able to say for sure.
Have you gotten lost in the myriad papers about protein spread, seeds, templated misfolding, and what to call a prion? You are not alone. Madolyn Rogers’ next installment of in-depth reports from the 12th International Conference on Alzheimer’s and Parkinson’s Diseases, held last month in Nice, France, puts it all into an up-to-date narrative for you. And what about those GWAS hits? What do they do, anyway? On this big question in current Alzheimer’s research, Rogers gathered news on some of the early GWAS finds, BIN1 and PICALM. In so doing, she came across—quelle surprise—the perennial debate of whether the effects in question work via tau or Aβ. Read this next-to-last installment of stories from Nice.
A study of almost 2 million people in the United Kingdom suggests that obese folk are one-third less likely to develop dementia than people of a healthy weight, while being underweight increases the risk by a third. While this news seems to dash hopes that controlling obesity will reduce dementia rates, experts warn that limitations to the study complicate its interpretation.
- Amy Nelson and Berislav Zlokovic on BMI and risk of dementia in two million people over two decades: a retrospective cohort study.
- Evgenia Salta and Bart De Strooper on Gene expression. MicroRNA control of protein expression noise.
- Bjørn Heine Strand on BMI and risk of dementia in two million people over two decades: a retrospective cohort study.
- Wiep Scheper and Jeroen Hoozemans on Phosphatase Inhibitor Promotes Protein Folding, Helps ALS Mice
- Anne Bertolotti on Phosphatase Inhibitor Promotes Protein Folding, Helps ALS Mice
- Emory Hill on Try This at Home: Cognitive Testing in the Age of Prevention Trials?
- Saak Ovsepian on Not All About Dendrites: Presynaptic Tau Harms Plasticity, Too