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.
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.
Co-sponsors Banner, Novartis, and Amgen announced that they will stop testing CNP520 in two Phase 2/3 studies in people at risk of AD. The drug worsened cognition.
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.
Longitudinal ADNI data tie higher sTREM2 in CSF to slower cognitive decline, reinforcing the idea that TREM2 activity protects the brain from AD pathology.
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?