Two phase III failures with Roche Holding AG subsidiary Genentech Inc.’s gantenerumab in staving off mild cognitive impairment tied to Alzheimer’s disease (AD) revealed the level of amyloid-beta removal was lower than the company expected. The protein amyloid beta accumulates in the brains of AD patients and its removal is suspected to be an eventual boon to AD patients. But there are still plenty of doubts. Top-line results from Genentech’s phase III Graduate I and II studies show gantenerumab, a fully human monoclonal IgG1 antibody, missed the primary endpoints of slowing clinical decline in those with mild cognitive impairment due to AD and mild AD dementia.
The University of Texas System and Massachusetts Institute of Technology (MIT) have synthesized transcription factor PU.1 inhibitors reported to be useful for the treatment of Alzheimer's disease.
Reduced expression of nuclear factor erythroid 2-related factor 2 (Nrf2) is observed in humans and animal models of Alzheimer’s disease (AD), with its activation being a promising therapeutic approach.
University of Calgary scientists described their work on a small peptide aptamer 8 to bind cellular prion protein and prevent its binding with β-amyloid oligomers, an interaction that activates tyrosine-protein kinase Fyn and neuroinflammation.
Sinaptica Therapeutics Inc. received a U.S. FDA breakthrough device designation for its electromagnetic therapy for Alzheimer’s disease. Sinaptistim-AD combines neurostimulation, brain wave monitoring and artificial intelligence (AI) to address the cognitive and functional decline in patients with the neurological disorder.
Tyrosine kinase SYK (spleen tyrosine kinase), an enzyme involved in immune signaling, could play a key role in Alzheimer's disease (AD), multiple sclerosis (MS), and other neurodegenerative diseases, according to a study from the University of Virginia (UVA). SYK regulates the activity of microglia, preventing the accumulation of secretions associated with AD or MS produced in these pathologies.
Increasing evidence exists regarding estrogen receptor β (ERβ) playing a protective role in Alzheimer’s disease (AD) and its loss resulting in progressive neural cell body degeneration.
