Researchers predict that a new BACE1 mouse recapitulates the early stages of sporadic Alzheimer’s, and can serve as a testing ground for BACE1 inhibitors.
Compounds that bind RNA temper toxicity related to ALS and FTD.
Connections across neural networks break down as cognition declines in people with different forms of AD, suggesting the wiring problems may be a hallmark of disease progression.
Researchers are ramping up efforts to target tau for Alzheimer’s and other tauopathies.
Blocking the microglial receptor for pro-inflammatory prostaglandin D2 protects motor neurons from glial toxicity in ALS cell and mouse models.
In gritty and sometimes harrowing detail, activist Meryl Comer describes the reality of caring for a loved one with Alzheimer’s disease.
Not the RNA aggregates, but the repeat dipeptides made from expansions in the C9ORF72 gene are responsible for neurodegeneration, a study claims.
Neurons derived from an octogenarian donor thrived in rat spinal cord lesions, extending thousands of axons along the length of the cord, even into the cortex.
After numerous disappointing trials of Alzheimer therapies that tackle Aβ, researchers are developing ways of targeting the peptide’s partner in crime, i.e., tau. As Alzforum wraps up coverage of the Alzheimer’s Association International Conference 2014, held July 12-17 in Copenhagen, Denmark, read how scientists are harnessing immunotherapy and anti-aggregation schemes to try to rid the body of the other pathological hallmark of AD.
- John Trojanowski on Therapies Take Aim at Tau
- Michael Sasner on Tau P301S (Line PS19)
- Ashkan Javaherian on Yeast Chaperone Melts Protein Aggregates
- Aaron Gitler on Yeast Chaperone Melts Protein Aggregates
- Jiou Wang on C9ORF72 Killer Dipeptides Clog the Nucleolus
- Jochen Herms on Alzheimer’s Disease: In the Eye of the Patient?
- Sylvie Claeysen on An antidepressant decreases CSF Aβ production in healthy individuals and in transgenic AD mice.