A series of novel tacrine derivatives acting as acetylcholinesterase inhibitors and N-methyl-D-aspartate (NMDA) receptor subtype antagonists has been developed in research seeking to exploit these targets for the treatment of Alzheimer's disease.
Researchers from the U.K. have investigated the specificity and sensitivity of clonidine growth hormone (GH) as a biomarker for the differential diagnosis of multiple system atrophy (MSA) from pure autonomic failure (PAF), Parkinson’s disease (PD) and progressive supranuclear palsy (PSP).
Recent efforts have unveiled UCB-0022 (UCB Pharma Inc.) as an oral, brain-penetrant small molecule acting as a selective D1 positive allosteric modulator.
Researchers from the University of Santiago de Compostela and University of Porto have reported the discovery of a novel acetylcholinesterase (AChE) inhibitor, MJM-255.
Iama Therapeutics Srl has sought new, selective inhibitors of solute carrier family 12 member 2 (NKCC1) to treat autism, Down syndrome and brain disorders featuring chloride (NKCC1/solute carrier family 12 member 5 [KCC2]) imbalance.
Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are two devastating neurodegenerative diseases, with clinical, pathological and genetic overlap, without effective therapy.
Therapeutic Solutions International Inc. has announced promising data on the use of Campbellcell for treatment of bipolar disorder by the company's suicide prevention-based spin-off Campbell Neurosciences Inc.
SBT-101 (Swanbio Therapeutics Inc.) is an adeno-associated virus serotype 9 (AAV9)-based gene therapy that delivers a functional copy of the ABCD1 gene and is under development for the treatment of adrenomyeloneuropathy (AMN).
As therapeutics development in Alzheimer’s disease (AD) is broadening its search for therapeutic targets, one of the alternatives to amyloid-β, or at least to its direct targeting by monoclonal antibodies, that is coming into focus is triggering receptor expressed on myeloid cells 2 (TREM2). From a drug development standpoint, amyloid-β remains a mystery. Scientific evidence clearly suggests that amyloid misprocessing is an underlying factor in the development of AD, and it is certainly a reasonable hypothesis that reducing amyloid plaque should fight the disease.