Does a Breached Blood-Brain Barrier Cause Seizures in AD?
Researchers link age-related weakening of the barrier to TGFβ signaling, hyperexcitation, and cognitive problems. In rodents, TGFβ antagonists attenuate these effects, reducing seizures.
Researchers link age-related weakening of the barrier to TGFβ signaling, hyperexcitation, and cognitive problems. In rodents, TGFβ antagonists attenuate these effects, reducing seizures.
While gene-based therapy for late-onset AD may seem distant, rare neurological disorders could point the way.
As gene therapy is making a comeback, scientists are exploring if it might prevent or reverse Alzheimer’s. Some of those treatments are permanent, heightening safety concerns.
Encouraged by success in treating infant spinomuscular atrophy, researchers are redoubling their efforts to target genetic causes of age-related neurodegeneration.
Specific patterns of expression defined distinct subtypes of neurons, astrocytes, oligodendrocytes, and microglia in this early affected brain region.
Brain biopsy tissue reveals that their transcriptomes shift by location, age, and disease.
In a mouse tauopathy model, knocking out the NLRP3 inflammasome prevented toxic tau from forming.
Based on preclinical data, researchers gave this antibiotic a shot in a two-year clinical trial. It did nothing to slow cognitive decline.
Alzforum encourages users to visit the Virtual Exhibit Hall, where companies showcase their newest initiatives, products, and services. We welcome F. Hoffmann-La Roche, joining our other exhibitors — Biogen, BioLegend, Dash Genomics, Inc., Abcam, BrainXell, and the Jackson Laboratory.
The success of using gene therapy to treat spinal muscular atrophy in babies has researchers eyeing neurodegeneration as their next target. From suppressing Aβ production to improving immunotherapy to regenerating lost neurons, the field is flush with new approaches. Could a single injection of billions of viral capsids slow or prevent Alzheimer’s, Parkinson’s, and other dreaded diseases?
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