Organoids patterned on the dorsal human forebrain consistently contain a set of cells native to the cerebral cortex, and develop along the same trajectory as fetal brains. Could they become the standard for organoid research?
In a mouse model of frontotemporal dementia, a trifecta of tau mutations hobbles newborn neurons in the dentate gyrus.
A PLCG2 variant that reduces a person’s risk of Alzheimer’s, frontotemporal dementia, and dementia with Lewy bodies also appears to extend longevity.
Phase 1b data show that Biogen’s BIIB092 lowers N-terminal tau fragments in cerebrospinal fluid by more than 90 percent.
Scientists link this mysterious form of dementia to higher plasma LDL-cholesterol, and to genetic variants in APOB, which encodes the major component of low-density lipoprotein.
Chemotherapy riles microglia, causing neurons to turn down expression of BDNF, a growth factor necessary for myelination. Restoring BDNF signaling on oligodendrocytes spared myelin and memory loss.
The locus incertus fine-tunes hippocampus neural activity to control memory formation in stressful situations. Could a new understanding of these circuits shed light on memory loss in Alzheimer’s?
Viral surfaces attract proteins from the extracellular environment of the person they infect. This corona of host proteins makes the virus more or less infective—and promotes amyloid fibrils.
New potential immunotherapies and insight into single-cell responses were highlights of a small meeting in Denmark.
Research on postmortem human brain strengthens the idea that an ebbing of neurogenesis may underlie cognitive decline.
Thousands of stretches of the genome go undetected by standard short-read sequencing techniques. Unmasking these “dark regions” revealed a potential AD risk variant in the CR1 gene.
Using single-nuclei or cell sorting, three separate research groups sequenced RNA from human postmortem brains. They unveiled AD-associated gene-expression signatures, but disease-related transcriptomes from human microglia were quite different from those in mice.
Antisense Oligonucleotides: Can They Take on ALS, SMA, Prions? American Academy of Neurology 2019 Annual Meeting ...
Data on ASOs, presented recently at the annual meeting of the American Academy of Neurology, depict RNA-based therapies as broadly on the rise in neurodegenerative diseases.
In a new, inducible mouse model, poly(GR) damages mitochondria, but its effect is reversible. In flies, turning off transcription of hexanucleotide expansion protects cells.