Dipeptide Repeat Proteins Don’t Directly Block Nuclear Transport
New data suggest that while peptides translated from an expansion in the C9ORF72 gene are toxic, they don’t directly interfere with nucleocytoplasmic transport.
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A Proteomics Dive into Cause of Frontotemporal Dementia
Proteomics and protein-protein interaction research may yield clues to etiology, tracking, and treatment of granulin-related and other forms of FTD/ALS.
Non-Amyloid Treatments: Inflammation, Epigenetics, Regeneration
A broadening drug development pipeline now contains Phase 1 or 2 drugs on targets unrelated to Aβ or tau.
Society for Neuroscience Annual Meeting 2019
Not Just Blood Pressure—Dietary Salt Linked to Tau Phosphorylation Time to Try Again: Gene-Based Therapy for Neurodegeneration Gene Therapies Enter Trials for Many Brain Pathologies—What about AD? Organized around 10 major themes, this year’s annual ...
At Least We Know These Don’t Work: Negative Trials at CTAD
Null results ended the development of the neuroprotective drugs edonerpic and abeotaxane, the AMPA receptor modulator S47445, and the dietary formulation tricaprilin.
First Round of FTD Therapeutics Fell Short, But Many More Are Up and Running
Researchers reported negative findings from three trials at ICFTD 2016.
Minocycline Does Not Work in Mild Alzheimer’s Disease
Based on preclinical data, researchers gave this antibiotic a shot in a two-year clinical trial. It did nothing to slow cognitive decline.
Experts Slam Marketing of Tramiprosate (Alzhemed) as Nutraceutical
The Canadian pharmaceutical company Bellus Health has begun to sell the would-be prescription drug tramiprosate over the counter as a nutritional supplement...
A Delicate Frontier: Human Microglia Focus of Attention at Keystone
Working with human microglia is fraught with technical challenges, but that didn’t stop researchers at Keystone from sharing a flurry of data on how these cells act in neurodegenerative disease.
Gosuranemab, Biogen’s Anti-Tau Immunotherapy, Does Not Fly for PSP
In PASSPORT study, the antibody failed to slow progressive supranuclear palsy. Alzheimer’s trial to continue.
Are Aβ Blood Tests Ready for Prime Time?
A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.
Move Over Aβ, CSF P-Tau Tells Us There’s Plaque in the Brain
At AAIC, researchers touted phospho-tau species, especially p217 and p181. They tick up in CSF as an early response to amyloid accumulation.
Move Over CSF, P-Tau in Blood Also Tells Us There’s Plaque in the Brain
At this year’s AAIC, no sooner had scientists reported that phospho-tau in the CSF might reflect early responses to amyloid, than they reported parallel data for phospho-tau in blood.
Synaptic Proteins in CSF: New Markers of Cognitive Decline?
Protein levels track with cognitive function and can distinguish Alzheimer’s patients from controls.
Blood Tests of Phospho-Tau, Aβ42, Track With Brain Amyloid
Using mass spectrometry to detect teensy amounts of phospho-tau species in plasma, researchers reported that p-tau-217 and p-tau-181 picked out people with Aβ pathology. Differences between groups appear to be huge. An MS-based test for plasma Aβ42 corresponded to brain amyloid, and is going in for regulatory approval.
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