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.
A chemist at the University of Cambridge, Dobson developed equations that described the kinetics of protein aggregation in diseases such as Alzheimer’s.
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.
Researchers induced cortical organoids to grow their own vasculature and even form a blood-“brain” barrier, making the little blobs more useful for studying disease.
The company halted its Phase 2 trial of ABBV-8E12 due to lack of efficacy.
By analyzing a single MRI scan, researchers pinpointed the origin of frontotemporal dementia pathology and predicted its future progression.
Longitudinal data identifies four stages of amyloid plaque buildup, with the earliest deposits appearing in the precuneus and posterior cingulate.
Functional variants of AD GWAS hits found in enhancers of myeloid genes.
These cells accumulate in old mouse and human hippocampi, as well as in a mouse model of neurodegenerative disease.
Longitudinal ADNI data tie higher sTREM2 in CSF to slower cognitive decline, reinforcing the idea that TREM2 activity protects the brain from AD pathology.
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.
Biogen and Eisai announced the discontinuation of the Phase 3 program. Elenbecestat was the only remaining BACE inhibitor being tested for AD.
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?