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.
By analyzing a single MRI scan, researchers pinpointed the origin of frontotemporal dementia pathology and predicted its future progression.
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.
Spewed by stressed microglia, fragments of the organelles provoke mitochondrial fission in other cells, causing astrogliosis and neuronal loss.
Resident T cells in the membrane surrounding the healthy mouse brain influence both short-term memory and synaptic plasticity.
A new study argues that the duration of a person’s amyloid positivity predicts whether they’ll develop tau accumulation and cognitive decline.
From more than 45,000 MRI scans, a typical pattern of brain aging emerges. Brains “age” faster in people who have a neurological disorder.
The G2019S variant that boosts Parkinson’s risk helps mice survive infection, but raises α-synuclein in the brain and increases neuronal death.
The circular transcripts correlate with AD pathology and dementia severity, suggesting potential roles in pathogenesis or as biomarkers.
The transcriptional repressor quiets neural activity and lengthens lifespan in worms. It is abundant in the brains of cognitively healthy centenarians.
Negative findings for AVP-786 belie positive findings from a separate Phase 3 trial announced earlier this year.
$73 million to transform big data into open-access targets and drugs for testing in clinical trials.