Herpesvirus: Trigger for Many Brain Pathologies?
At Quebec conference, researchers considered multiple aspects of herpesvirus biology that may come in to play in AD.
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At Quebec conference, researchers considered multiple aspects of herpesvirus biology that may come in to play in AD.
Much of the neuron loss in rTg4510 mice comes from accidental disruptions in mouse genes rather than expression of mutant tau. Pathology spreads quickly in human tau knock-ins.
A U.K. research program developed guidelines for clinical practice. In preliminary studies, it boosted diagnosis and improved patient care.
The field is rapidly building the infrastructure for biomarker studies and large clinical trials.
The field is searching for a combination of clinical features and biomarkers that will identify the disease in people with mild cognitive impairment.
Longitudinal data identifies four stages of amyloid plaque buildup, with the earliest deposits appearing in the precuneus and posterior cingulate.
Middle-aged people who exercise more are less likely to become amyloid-positive. In late life, people with brain amyloid who exercise declined more slowly and had less brain shrinkage over the following years.
In mice, the back of the brain, near the neck, contains lymphatic vessels that are specialized to take up cerebrospinal fluid and deliver it to cervical lymph nodes.
The company halted its Phase 2 trial of ABBV-8E12 due to lack of efficacy.
Analysis of a chimeric mouse shows that the cells express the same genes they do in the human brain, survey their environment, and respond to injuries and amyloid.
A brother’s survival guilt, a journalist tracing her mutation to Lebanon, a student freezing her eggs ahead of a primary prevention trial—DIAN family members are stirring their growing community to act against Alzheimer’s disease.
Nearly 30 years after the first Alzheimer’s gene discoveries, genetics once again drives recruitment, scientific progress, and therapy development in the Dominantly Inherited Alzheimer’s Network.
RPS25 helps translate repetitive snippets of RNA that are associated with neurodegenerative diseases. Knocking it down reduces protein aggregates and cell death.
As the Alzheimer’s field suffers smackdowns in trials of small molecules and antibodies, antisense oligonucleotides are quietly coming along—and looking safe so far.
Too much or too little serum hemoglobin increases risk for Alzheimer’s and other dementias by 20 percent or more.
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