As SPRI Clinical Trials of Brooklyn continues to work aggressively on behalf of pharmaceutical companies on a number of Memory Loss Clinical Research Studies Brooklyn in hopes of finding new ways to provide symptomatic relief of memory loss due to Alzheimer’s disease, news of attempts to slow the progression of this disease hits a major setback.

Eli Lilly reported last week that its experimental Alzheimer’s drug, solanezumab, failed to slow the progression of memory loss associated with Alzheimer’s disease in a large recently completed clinical trial.  As a result, it has been reported that Eli Lilly will discontinue development of this drug as a means of attempting to modify disease progression due Alzheimer’s disease.

The drug belongs to a class of drugs that works by impeding the formation of amyloid plaques in the brain.  It has been widely thought that the production of amyloid plaques is a key underlying factor to both disease progression and thesubsequentdecline in memory and cognitive functioning that occurs during Alzheimer’s disease.  Eli Lilly is not the only company exploring ways to slow the production of amyloid plaques within the brains of Alzheimer’s patients, but these results are sure to cause concern within the medical research community about the potential for this approach to reverse or slow the progressive deterioration in cognitive functioning that occurs in patients already expressing memory loss due to Alzheimer’s disease.

A growing number of researchers believe, however, that by the time a person becomes symptomatic, it is already too late for the approach Lilly and other drug companies are trying.  It is now well known that abnormal production of amyloid begins to occur within the brainsof Alzheimer’s patients as much as a decade or more before even the first symptoms of the disease manifests itself.   This poses a significant challenge because it suggests that a better approach to the treatment of Alzheimer’s disease is to attempt to affect the underlying disease process before people actually show signs they have the disease.  But how would onerealistically test such a hypothesis without knowing who was actually at risk of developing the disease?

It turns out there may be a way.  It is known that there are actually two forms of the disease – one that first manifests itself after the sixth decade of life and a second that begins to manifest itself much earlier in life – as early as age 40.  While it is not clear what factor(s) trigger the disease in those who begin to show signs of the disease later in life, it is clear that a mutation in a specific gene(s) is responsible for the early onset form.  Scientist have identified a group of people living in Columbia South America who are all related and have an abnormally high incidence of contracting this early onset form of Alzheimer’s disease.  Testing of this extended family has revealed that all of those who go on to develop dementia have a mutation in a specific gene that is known to cause increased production of amyloid.  A major research study is now underway, funded by Genetech, the National Institutes of Health and other parties to see if treating this group of people will reduce the incidence of the development of Alzheimer’s dementia.  While the answer to this question is still many years away, it does represent an ideal way to find out if the way to treat this disease is before it actually overtly manifests itself.