At Keystone, the work of several groups painted TREM2 as a dedicated supporter of microglial function across neurodegenerative disease models, including those for ALS.
Screen identifies antibody that induces mouse bone marrow cells to differentiate and travel to the brain, where they clear plaques.
A majority of amyloid PET scans led physicians to change how they managed a patient’s disease. The effect on later outcomes is yet to be come.
Transcranial, alternating electrical current restored neuronal synchrony in older people, rejuvenating working memory. For an hour or two.
Subgroup analysis addresses APOE4 randomization imbalance, claims treatment with this anti-Aβ protofibril antibody slowed cognitive decline.
Hunting for rare mutations that cause dementia, researchers have spotted, but not yet snagged, some tantalizing candidates.
The May 26 Nature Neuroscience online debuts 25 new candidate genes for amyotrophic lateral sclerosis...
After years of grunt work on next-gen sequencing and expression analysis, geneticists are finally reaping results. The new genes underscore the role of known pathways and cell types in disease.
Presented at AD/PD, the discovery by scientists in Uppsala is the first APP deletion found to cause Alzheimer’s disease. The same group found the Swedish and Arctic APP mutations.
Long-term treatment with the anti-sense oligonucleotide led to motor benefits in an extension trial of children 2 to 15 years old.
Diagnostics Accelerator to fund projects that develop dementia biomarkers from patient data.
People who take leisurely walks, garden, and tackle household chores had bigger brains than those who were more sedentary. Vigorous exercise brought neither additional benefit nor harm.
At a Keystone meeting, researchers agreed that ApoE stokes damaging neuroinflammation in response to tau pathology. The E4 allele ramped up cholesterol biosynthesis in microglia and astrocytes, and even promoted neuronal damage when expressed outside of the brain.
By aging cultured neurons and manipulating them to stimulate endocytosis or interfere with vesicle release, researchers can bring about characteristics of Alzheimer’s—without adding APP or Aβ.
Researchers no longer debate whether misfolded proteins spread through the brain in neurodegenerative disease. Now they want to know how.