Injecting a piece of this anti-aging protein days before memory testing improved performance in mice young and old, as well as those that overexpress α-synuclein.
High-throughput sequencing yields surprises. Learn about pathogenic variants in endosomal genes, an algorithm to nab the worst SORL1 mutations, dominant PS1 mutations arising de novo, and tau duplications.
Researchers at AAIC reinforced the idea that tau pathology drives cognitive decline, although amyloid plaques were implicated in semantic memory deficits.
Researchers at AAIC described different correlates of CSF and PET measures of Aβ and tau.
Report details ways to improve care of people who have dementia, argues for societies to implement ambitious prevention strategies, but offers only reduction of hypertension as a plausible intervention.
Scientists at AAIC described a large, multidomain intervention trial in the United States to test if lifestyle changes can stave off cognitive decline. YMCAs nationwide are in on the project; similar trials are in the works in other countries.
TREM2 knockout causes a metabolic meltdown in microglia, but treating mice with cyclocreatine restores ATP levels and rejuvenates the cells to fight amyloid.
Findings from a 25-year longitudinal study in a large, biracial cohort point to preventable mid-life vascular problems as a top dementia risk factor.
Biomarkers provide a glimpse into disease pathology, but researchers are still learning how to interpret what they see. At AAIC, speakers emphasized that PET scans and cerebrospinal fluid markers reflect distinct aspects of disease and thus are not interchangeable. Other talks tied tau tangles more closely to cognitive decline, and implicated amyloid plaques in precipitating a specific deficit in semantic memory.
A consensus report commissioned by The Lancet, and debuted at this year’s AAIC meeting in London, claims that a third of dementia cases could be avoided. “Be ambitious about prevention,” the report urges. Treating midlife hypertension gets top billing among a list of actions that might delay dementia. Beyond prevention, the report lists recommendations that could substantially improve intervention and care for patients right now.
A new study suggests a reason why loss-of-function mutations in TREM2 increase the risk for late-onset Alzheimer’s. Loss of TREM2 saps the fighting spirit of microglia, causing a metabolic meltdown that depletes the cells’ energy and leads to apoptosis. Treating mice with cyclocreatine prevented this energy deficit, and the cells once again shielded the brain from amyloid toxicity. Would finding better ways to support microglia help fight the progression of AD?
The Alzheimer’s field has been inching toward a prevention model, with several trials starting to target presymptomatic stages of the disease. At AAIC 2017, researchers set their sights higher, arguing that the time has come for a true primary prevention trial. Young adults who carry familial AD mutations will take BACE inhibitors to find out if suppressing Aβ production can stop plaques from forming in their brains.
The idea that toxic amyloids form strains, much like prions, has raised fundamental questions about Alzheimer’s and other neurodegenerative diseases. What is the smallest structure that retains the quintessential properties of these strains? How many different strains exist? How many can occur in a single brain? At AAIC 2017, scientists had some surprising answers.
- Edo Richard on New Dementia Trials to Test Lifestyle Interventions
- Axel Montagne, Mikko Huuskonen and Berislav Zlokovic on Ring Around the Vessel: Enlarged Spaces Signal Vascular Disease
- Jaime Grutzendler on Without TREM2, Microglia Run Out of Gas
- Mary Beth Humphrey on Without TREM2, Microglia Run Out of Gas
- Christian Haass and Gernot Kleinberger on Without TREM2, Microglia Run Out of Gas
- Costantino Iadecola on Vascular Problems in 40s, 50s Beget Dementia Down the Road
- Gary Landreth on Searching for New AD Risk Variants? Move Beyond GWAS
- Christian Haass and Gernot Kleinberger on Searching for New AD Risk Variants? Move Beyond GWAS
- Johnathan Cooper-Knock on Searching for New AD Risk Variants? Move Beyond GWAS
- Eric McDade on CRISPR Edits Genome of Human Embryos
- Marc Dhenain on As Youth Fades, So Does the Fire of Glycolysis in the Brain
- Gwenaelle Douaud on As Youth Fades, So Does the Fire of Glycolysis in the Brain
- Richard Caselli on As Youth Fades, So Does the Fire of Glycolysis in the Brain
- Eric M. Reiman on As Youth Fades, So Does the Fire of Glycolysis in the Brain
- Norman Foster on In Clinical Use, Amyloid Scans Change Two-Thirds of Treatment Plans
- Kejal Kantarci on In Clinical Use, Amyloid Scans Change Two-Thirds of Treatment Plans
- Stephen Salloway on In Clinical Use, Amyloid Scans Change Two-Thirds of Treatment Plans
- Joel Ramirez and Sandra Black on Ring Around the Vessel: Enlarged Spaces Signal Vascular Disease
- Rebecca Gottesman on Ring Around the Vessel: Enlarged Spaces Signal Vascular Disease
- Mariko Bennett on New Technology Catalogues Immune Cells in Brain
- Johannes Levin on Revised Guidelines for Diagnosing Progressive Supranuclear Palsy