COMMENTARY New therapies for Alzheimer’s offer hope
Alzheimer’s disease is expected to affect an estimated 14 million American by the year 2050, and while there are medications that improve symptoms and slow decline for a brief period, the search continues for ways to prevent as well as to counteract the onslaught of neurodegenerative progression that so mentally, emotionally and physically devastates families who are touched by its horrific effects. Advances in many fields — genetics, molecular biology and bioengineering — now offer new findings that are cause for cautious optimism. The current paradigm is that in AD devastating brain changes result from the interaction of several factors, and many cutting edge drug therapies are focusing on one aspect of causation with the intent to disturb the chain of processes that ends in dementia. According to the October 2007 issue of “ Mind, Mood, and Memory,” published by Massachusetts General Hospital, the following represent five of the most promising new drugs worth keeping track of as they progress through various stages of clinical trials.
Alzhemed interferes with the amalgamation of plaque in the brain ( a hallmark of those with AD) and inhibits inflammatory responses associated with such accumulation. Results of controlled, randomized trials involving large groups of patients are now being assessed in anticipation of public release.
Flurizan lowers the production of an amino acid involved in the formation of a toxic protein. In small trials ( groups of up to 300 people), this drug, at high levels, has been shown to improve overall functioning in cases of mild AD. Randomized trials involving large groups of patients are currently in progress.
Ketasyn provides an alternate energy source to the cells using ketone bodies to replace scarce glucose. In AD, neurons are damaged by a decline in levels of glucose, which supplies energy to cells. Taken as a drink each morning, it has proven effective in significantly slowing disease progression in those without genetic predisposition to AD.
Dimebon protects brain cells from processes associated with cell death. After six months, those who received the drug improved significantly in cognitive function, memory, ability to perform tasks of daily living, global function and behavior as compared to those who received a placebo. Longer trials are underway to assess effectiveness and safety over time.
Rapineuzumab shows promise in terms of attaching to plaque tithing the brain and eliminating it from the body. Trials using small groups of up to 300 patients each are in progress.