The latest hoped-for breakthrough drug in the fight against Alzheimer’s has been scrapped. But all is not quite as bleak as it might seem: drugs like bapineuzumab might still prove useful as an early intervention vehicle, possibly preventing plaques from forming and building up in the brains of individuals who show early signs of cognitive problems thought to be precursors of Alzheimer’s.
It was with considerable disappointment that Johnson & Johnson pharmaceuticals recently announced through a press release and on its website the suspension of further clinical trials of a drug many had hoped would herald a new age in the treatment of mild-to-moderate Alzheimer’s Disease. The drug, bapineuzumab, is administered intravenously and is one of a new class of drugs designed to more directly target and wipe the brain clean of the beta-amyloid plaques thought to play a central role in the disease. But at both stages of its clinical trials, the drug failed to perform better than a placebo, and given the risks involved in treatment as well as the lackluster results, clinical trials were suspended.
Although the results of recent bapineuzumab testing are not what many had hoped for, the future of the drug might not be as bleak as some fear. Alzheimer’s researchers have long known that regardless of the role beta-amyloid plaques play in the development of the disease, the progressive nature of the disease and the worsening of symptoms over time make it a considerable challenge to treat, even if a drug is found that successfully attacks and removes the underlying cause. The damage done to the brain’s nerve cells and their inter-cell communication network might be such that even successfully removing the plaques thought to play a key role in that damage might not be sufficient to reverse the harm already done. That’s why some researchers are suggesting that it’s possible that drugs like bapineuzumab might still prove useful as an early intervention vehicle, possibly preventing plaques from forming and building up in the brains of individuals who show early signs of cognitive problems, including those with conditions thought to be precursors of Alzheimer’s Disease. If in fact plaque build-up is crucial to the development of full-blown Alzheimer’s, and if that buildup can be prevented, then perhaps drugs that prevent plaque formation or remove plaques which have already formed can prevent the development of the disease or prevent those suffering from milder forms of cognitive dysfunction from progressing to Alzheimer’s. And even if amyloid plaques turn out not to be the principal cause of Alzheimer’s — it is already known that various enzymes, proteins, genetic variations, and other factors contribute not only to the disease process but also to the development and influence of plaques — factoring out their influence in those afflicted with Alzheimer’s could shine a much brighter light on the other factors that play key roles in the disease.
Although Alzheimer’s Disease is the most common form of dementia, affecting an estimated 35-40 million people worldwide, we now know that cognitive impairments lie along a continuum, with Alzheimer’s being the most comprehensively debilitating cognitive spectrum disorder. Other conditions, such as Mild Cognitive Impairment (MCI), can also significantly impact a person’s ability to remember and to carry out daily activities. And many, but not all individuals with conditions like MCI eventually get diagnosed with Alzheimer’s. But as the world’s population continues to age and as a greater proportion of that population experiences some form of cognitive decline, the stress put on the health care system and its resources is increasing exponentially. So, there’s plenty of motivation to continue a robust search for a cure. And despite this most recent setback, there’s still much hope that interventions targeting the formation of beta-amyloid plaques will prove crucial to the fight against Alzheimer’s and the broad spectrum of cognitive impairment disorders.
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