MGH meeting traces arc of scientific discoveries from 1980s to today’s cutting edge.
Older people who complain of memory problems are more likely to become measurably impaired and to have Alzheimer’s pathology in the brain, especially if they smoke or carry an ApoE4 allele.
Protein oligomers may be to blame in TDP-43 proteinopathies, as in other neurodegenerative conditions.
Researchers have partnered with Google-funded Calico Life Sciences to develop a molecule that protects neurons in a variety of conditions.
Starved for a protein that regulates lipids, neurons suffer and Aβ production soars, according to a new study.
In narrower claim, the drug is said to promote ApoE lipidation only in brain regions with extensive amyloid in mice carrying human ApoE4.
Data suggest Aβ-dependent and –independent pathways combine forces to compromise cognition in otherwise healthy people.
Neural circuits in the hippocampus defy current views about its structure and function.
As the first five of the nation’s 27 Alzheimer’s Disease Research Centers system mark their 30th birthday, one of them celebrated with a scientific conference at Massachusetts General Hospital. Blending the past, present, and future, scientists told stories of how the discovery of the first presenilin mutation today lives on in structural work to find better γ-secretase drugs, or how an overlooked gel band visible since the 1990s now hints at an unappreciated APP cleavage and adds a new twist to explore in BACE1 inhibitor drugs. Others summarized the latest on characterizing the Alzheimer’s prodrome and sharpening tools to target it in secondary prevention trials. Along the way, conference attendees learned that, laid out flat, the cortical mantle of the human brain is the size of a large pizza, a factoid that matters to understanding Alzheimer’s. Read on.
So you thought you knew the hippocampus? Think again. New studies illuminate nuances of this ostensibly familiar structure that may come as a surprise. Axons spring from unusual places and extend in multiple planes, while synaptic oscillations pulse along an unexpected path.
Dilute them to infinitesimal concentrations. Fix them in formaldehyde. No matter, Aβ from Alzheimer’s brain still seeds plaques in mice, according to recent reports. This astonishing tenacity emphasizes the prion-like nature of Aβ seeds. And yet, robust as they may be, these seeds appear to stay inside brain tissue since they are oddly absent from the cerebrospinal fluid. The new findings underscore profound differences between Aβ species in the brain parenchyma and the cerebrospinal fluid.
- Sylvia Villeneuve on Synergistic Effect of β-Amyloid and Neurodegeneration on Cognitive Decline in Clinically Normal Individuals.
- Radosveta Koldamova on Amyloid-β Pathology and APOE Genotype Modulate Retinoid X Receptor Agonist Activity in vivo.
- David Wolk on Synergistic Effect of β-Amyloid and Neurodegeneration on Cognitive Decline in Clinically Normal Individuals.
- Eric M. Reiman on Synergistic Effect of β-Amyloid and Neurodegeneration on Cognitive Decline in Clinically Normal Individuals.
- Gael Chetelat on Synergistic Effect of β-Amyloid and Neurodegeneration on Cognitive Decline in Clinically Normal Individuals.
- Daniel Michaelson on Amyloid-β Pathology and APOE Genotype Modulate Retinoid X Receptor Agonist Activity in vivo.
- Claudio Soto on Bad Seeds—Potent Aβ Peptides Instigate Plaques, Won’t Be Fixed