AD Clinical Pipeline: Immunotherapy Woes, Dimebon Boons
Two papers in the 19 July Lancet bring both dismay and hope to the ongoing quest for more effective AD treatments...
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Two papers in the 19 July Lancet bring both dismay and hope to the ongoing quest for more effective AD treatments...
Are high-molecular-weight, multi-protease complexes cellular Aβ factories?
One of the earliest signs of amyloid-β (Aβ) toxicity is synaptic loss, and recent work from a number of labs has shown that...
A lively platter of slide talks on APP processing and β-secretase (BACE) activities yielded a few interesting tidbits on the...
They are no match made in heaven, but in neurons, the two proteins responsible for amyloid plaques and neurofibrillary tangles might...
The transcriptomes of single immune cells in the mouse brain identify specific disease-associated microglia (DAM), which eat away at Aβ deposits.
Scientists propose that LATE is a neurodegenerative disease marked by TDP-43 pathology in limbic regions, and memory loss. After death, it can be seen alone or with other pathology.
Middle-aged WTC responders have cognitive problems, which correlate not only with their PTSD symptoms and exposure to toxic dust, but also with biomarkers of amyloid and tau.
In the human brain, alpha waves fell out of sync, while delta-theta waves swelled in concert with amyloid plaques, neurofibrillary tangles. Alpha modulation correlated with cognitive decline.
When the agency sent warning letters to 17 companies that falsely advertised cures and preventions for AD, most took down exaggerated claims. But can regulations stay ahead of the market?
Feeling good on the outside often helps us feel good on the inside. Could the same be true for neurons?...
Two papers advance the drive to develop an Alzheimer's vaccine, one looking at the antibody response in some of the Elan trial participants, the other using sophisticated methods to analyze the epitope recognized by antibodies generated in response to Aβ42 immunization.
Researchers induced cortical organoids to grow their own vasculature and even form a blood-“brain” barrier, making the little blobs more useful for studying disease.
In female mice it’s the other X chromosome, not lack of a Y, that extends life and preserves memory in the face of amyloidosis. A histone demethylase gene partly explains this. It protects people, too.
The antiviral protein enhances γ-secretase processing of APP. More of it is present in Alzheimer’s disease.