neuroscience, neurodegeneration, disease & medicine

Manipulating the production of new neurons can improve cognition in animal models of the disease, raising the possibility that figuring out a way for humans to make more neurons could make a difference for people with dementia.

The variant causes a buildup of BACE1 protein in axons in cultured neurons and mice. Researchers say it might be time to rethink failed trials that inhibit BACE1 to treat the neurodegenerative disease.

The test will be a cheaper and more accessible alternative to currently available diagnostic tools, researchers say.

After six months, patients with fast-progressing amyotrophic lateral sclerosis who had received the experimental treatment had less loss of function than those who received a placebo.

New studies show that elevated levels of a form of tau called p-tau217 can accurately distinguish Alzheimer’s disease from other forms of dementia, and perhaps even predict it.

The cell conversion strategy restores neurons and motor functions lost as a result of an induced Parkinson’s-like illness in the animals.

While the findings contradict previous studies that have linked human herpesvirus 6 to the neurodegenerative disease, they do not eliminate the possibility of a relationship.

This year’s most beautiful illustrations covered topics including the molecular underpinnings of Parkinson’s disease and strategies for tracking marine organisms around the world’s oceans.

A look at some of the circulating molecules that may indicate various Alzheimer’s pathologies and serve as the bases of noninvasive tests for the disease.

Researchers hope circulating biomarkers will enable earlier detection and better monitoring of the neurodegenerative disorder—and perhaps help usher in new treatments.

Evidence is accumulating that breathing contaminated air might impair cognition.

Contaminants in the atmosphere appear to have harmful effects on neurodevelopment and cognitive function.

A growing body of evidence supports the theory that neural hyperactivity and hyperconnectivity precede the pathological changes that lead to neurodegeneration.

Damage to the lysosome, the organelle that removes excess proteins, lipids, and other materials, might be at the root of the disease.

Patients who suffer a traumatic brain injury may exhibit abnormally abundant tau protein many years later, a new in vivo imaging technique reveals.

Mutations within the MS4A gene cluster have been linked to changes in protein levels that affect disease risk.

Boosting the levels of Akkermansia muciniphila in mouse guts slowed the progression of an ALS-like disease, while two other microbiome members were associated with more severe symptoms.

Johns Hopkins’s Ted Dawson discusses his lab’s demonstration that misfolded α-synuclein can move from the stomach to the brain and cause physical and cognitive symptoms.

Exposing mice to an hour of 40-hertz stimuli every day for a week reduced levels of amyloid-β plaques and tau protein, and improved cognition.

Pathogens can take various routes to pass the blood brain barrier and damage cells.