So you think Alzheimer’s is a neuronal disease? Well, yes, but you might as well think again. Even as the amyloid hypothesis is growing stronger with human genetics and longitudinal biomarker studies, decades of neurocentric research have given way to a broader appreciation that Aβ and tau intersect with the glial and vascular system and are subject to new forms of genetic regulation in the aging brain. What’s more, parabiosis shows that the blood itself carries signals into the brain that can powerfully influence its aging and degeneration. These topics dominated the first Zilkha Symposium on Alzheimer’s Disease and Related Disorders, hosted on April 4 by the University of Southern California. Gabrielle Strobel’s series covers the meeting highlights.
Baby Boomers, keep your blood pressure down. Research is beginning to explain how even mild hypertension, a mid-life risk factor for late-life dementia, might be damaging the neurovascular unit.
Do blood components really leak across an inflamed blood-brain barrier early on in the development of Alzheimer’s disease? Some GWAS hits and budding neuro-imaging and fluid markers are helping researchers find out.
The overused adage of the fountain of youth rears its head again, as four new studies show how young blood rejuvenates old brain and muscle, pumping up the vasculature, stem cells, and restoring microglia’s appetite for waste products. Researcher are isolating the responsible factors, for example GDF11.
Researchers are increasingly branching out from their old focus on Aβ and tau to understand how these proteins intersect with physiological processes and new genetic regulatory mechanisms in the aging brain.