Recent experimental work indicates that Glycadia’s compound in clinical development for vascular complications of diabetes may have efficacy in Alzheimer’s disease. The drug significantly lowered levels of the amyloidogenic AB42 peptides in the brains of transgenic mice expressing the human Amyloid Precursor Protein, an experimental model of Alzheimer’s disease.
Alzheimer’s disease, the most common form of age-related dementia, affects approximately 5 million people in the US and is expected to afflict increasing numbers as the boomer generation ages. Patients with Alzheimer’s disease have a progressive loss of mental and physical function, with clinical manifestations that include agitation, indifference, disorientation, memory loss, delusional thinking, inability to verbalize thoughts, language deterioration, and eventual aphasia, disablement, and immobility. Pathological manifestations include abnormal clumps of protein, known as amyloid plaques, and tangled bundles of nerve fibers, known as neurofibrillary tangles. Current treatment provides at best only modest symptomatic relief and does not address underlying abnormalities responsible for the disease, but there is substantial effort to identify new agents with novel mechanisms that can do so. Anti-amyloid intervention is one of the main potential therapeutic strategies.
Clinical Experimental Pharmacology & Physiology 36:1099-1103, 2009
Reduction of Aß42 in brains of transgenic APPswe mice by 2-3-chlorophenylaminylacetate