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.
The first ever cryo-EM structures of Aβ fibrils extracted from AD tissue look quite different than prior structures of fibrils generated in vitro. For starters, they are right-hand twisted, not left-hand.
Imaging studies suggest that ApoE4 carriers may be more susceptible to the effects of tangles, particularly if they are women.
Aβ oligomers latch onto adrenergic receptors, mobilizing a kinase that phosphorylates tau. Blocking adrenergic signaling wards off memory problems in amyloidosis mice.
Functional connections between two brain regions are the strongest indicator that pathologic, accumulated tau will spread from one to another.
The cells are primed to attack. Their targets include Epstein-Barr virus peptides.
A flavonoid reportedly spices up oxidative phosphorylation in microglial mitochondria, revving up phagocytosis of amyloid plaques in mouse models. The small study needs independent replication.