Using a collection of isogenic iPSC-derived neurons harboring different familial AD mutations, researchers found that, across the board, the mutations meddled with endosomes via elevated β-CTF.
Desikan pioneered advances in neuroimaging and neurogenetics, and was known for his passion and collaborative spirit.
In mice, the back of the brain, near the neck, contains lymphatic vessels that are specialized to take up cerebrospinal fluid and deliver it to cervical lymph nodes.
The company halted its Phase 2 trial of ABBV-8E12 due to lack of efficacy.
Longitudinal data identifies four stages of amyloid plaque buildup, with the earliest deposits appearing in the precuneus and posterior cingulate.
Hypertension in people as young as the mid-30s can predict late-life cerebrovascular disease and brain shrinkage. Intensive reduction of blood pressure can prevent the damage, but not when given in late life.
These cells accumulate in old mouse and human hippocampi, as well as in a mouse model of neurodegenerative disease.
Functional variants of AD GWAS hits found in enhancers of myeloid genes.
New evidence suggests the dimers impede clearance of glutamate from synapses, contributing to the hyperexcitability seen early in Alzheimer’s disease.
The phenotype of ApoE4 astrocytes and microglia resembles that of these cells in Alzheimer’s brain. Could defects in lipid metabolism and the extracellular matrix bring on the disease?
In vicinity of plaques, astrocytes and glia change gene expression in concert.
Analysis of a chimeric mouse shows that the cells express the same genes they do in the human brain, survey their environment, and respond to injuries and amyloid.
Middle-aged people who exercise more are less likely to become amyloid-positive. In late life, people with brain amyloid who exercise declined more slowly and had less brain shrinkage over the following years.
RPS25 helps translate repetitive snippets of RNA that are associated with neurodegenerative diseases. Knocking it down reduces protein aggregates and cell death.
Too much or too little serum hemoglobin increases risk for Alzheimer’s and other dementias by 20 percent or more.