Insight into the pathomechanics behind Alzheimer's disease (AD) continues to rise and a number of recent articles here on AAAS MemberCentral have focused on the condition (see below for links). There are 2 main reasons why this disease receives so much attention: it is the most common form of dementia, and there is no cure for its progressively fatal course.
Though a number of plausible hypotheses remain at the present time with regards what causes the disease, it is clear that the accumulation of β-amyloid (Aβ) plaques in neurons is likely to play a role in the pathomechanics of the condition, and particularly, in the disruption of synaptic functioning.
In a recent article published online by Science Express, the authors discuss a unique trial in mice in which a drug called Bexarotene was used to increase the degradation of Aβ. Administration of Bexarotene resulted in remarkable reduction of Aβ (Aβ40 and Aβ42) levels in brain interstitial fluid (ISF) of mice within 6 hours, with a 25 percent reduction by 24 hours. Indeed, acute treatment also resulted in a reduction of both diffuse and compact Aβ plaques in the cortex of the hippocampus.
In their research note, the authors describe augmented cognitive function and social behavior in mice after treatment with Bexarotene and state "The improved behaviors observed in bexarotene— treated mice suggest global improvements of neural network function."
Though these findings must first be replicated in humans to evaluate their potential efficacy, the study demonstrates a unique possibility for the development of a new line of therapeutics which can improve the underlying pathology. Conversely, current medications, such as acetylcholinesterase inhibitors (rivastigmine), function rather to augment the performance of the neurons and do not tackle the diseases progressive nature. Therefore, I am particularly intrigued by these findings and would recommend interested AAAS members to take advantage of their access to the article to check it out.