According to new research, as both mice and humans grow older, immune signals change at the interface between blood and cerebrospinal fluid.
Perfectly healthy mitochondria can sicken neurons simply by being in the wrong place.
A man lacking ApoE appears to have no cognitive deficits, and his brain and CSF biomarker profiles appear normal. Some claim the findings support ApoE as a rational drug target for AD.
The first large-scale surveys of DNA methylation in Alzheimer’s brains turned up numerous altered regions that may point to new genes involved in pathology.
Researchers predict that a new BACE1 mouse recapitulates the early stages of sporadic Alzheimer’s, and can serve as a testing ground for BACE1 inhibitors.
Compounds that bind RNA temper toxicity related to ALS and FTD.
Connections across neural networks break down as cognition declines in people with different forms of AD, suggesting the wiring problems may be a hallmark of disease progression.
Researchers are ramping up efforts to target tau for Alzheimer’s and other tauopathies.
Could age-related changes in the choroid plexus, the structure that produces cerebrospinal fluid, contribute to brain aging? As mice and humans reached old age, immune signals from the structure appeared to lean toward a type I interferon response. In mice, dialing back those signals to levels found in younger animals boosted memory and neurogenesis, while quieting inflammation. Scientists believe the findings reveal new mechanisms controlling aging in the brain.
- Masato Mitsuhashi on Exosomes Stand Out as Potential Blood Biomarkers
- Daniel Michaelson on Effects of the Absence of Apolipoprotein E on Lipoproteins, Neurocognitive Function, and Retinal Function.
- Gary Landreth on Effects of the Absence of Apolipoprotein E on Lipoproteins, Neurocognitive Function, and Retinal Function.
- Leon Tai, Manel Ben Aissa and Mary Jo LaDu on ApoE: One Man’s Brain Can Do Without It
- Suzana Petanceska on Alzheimer’s Brains Mottled with Epigenetic Changes
- Samantha Budd on Knock-In of Human BACE1 Cleaves Murine APP and Reiterates Alzheimer-like Phenotypes.
- Stefan Lichtenthaler on Knock-In of Human BACE1 Cleaves Murine APP and Reiterates Alzheimer-like Phenotypes.