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?
The protein forms cohesive rafts along microtubules, protecting them from digestion and regulating movement of molecular motors.
Eliminating microglia in a mouse model of amyloidosis nearly abolished parenchymal plaques, but led to a huge buildup of amyloid in cerebral blood vessels.
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?
The organelles express unique sets of proteins depending on their environment. Astrocyte mitochondria process lipids better than those in neurons.
New data strengthen the idea that a healthy locus coeruleus keeps memory sharp into old age.
In induced human microglia, the E4 allele profoundly affected their health and cellular responses, while familial Alzheimer’s mutations had little effect.
Sedentary mice infused with the plasma of active ones had more newborn neurons in the brain and less neuroinflammation. Exercising upped plasma clusterin in mice and in humans.
Hypometabolism in the frontal cortex and in the anterior default mode network distinguish the behavioral variant of AD from typical AD.
Overexpressing neuronal A2A receptors stoked C1q in microglia, damaging synapses and memory.
Ablating the immune cells protected mouse models of frontotemporal dementia from the neurodegeneration caused by human ApoE4.
Amyloid plaques in postmortem human cortex correlated with the proportion of microglia that were activated, not with microglial numbers. Tau pathology and cognitive decline come later.
Serial amyloid and tau scans in cognitively healthy people indicate that the speed at which a person’s tau accumulates best predicts his or her future cognitive decline.
An electron microscopy study reveals a jumbled mess of membrane chunks and malfunctioning organelles, bound together by phosphorylated or truncated α-synuclein.
In vicinity of plaques, astrocytes and glia change gene expression in concert.