Alzheimer’s – Prevention May Be the Answer

By 2030, more than 70 million people worldwide are expected to have Alzheimer’s, at a global cost of US $2 trillion. Yet, treatment for this disease has remained as elusive as ever.

Adapted from Eric McDade and Randall Bateman in Nature, July 2017

Unless there is a breakthrough, one in every 2-3 people over the age of 85 will have Alzheimer’s. Initially, clinical trials had focused on the treatment after the development of symptoms such as memory and speech impairment. In the past five years, trials have been done before the onset of symptoms when brain scan reveal the presence of amyloid -β protein plaques. The time has now come, the authors suggest, to stop the disease before any brain pathology even appears.

Alzheimer research dates back to the 1980’s when the NIH got in the game with major funding of Alzheimer’s Disease Centers. Since the last 20 years, research has focused on removing the amyloid -β plaques and tau tangles (neurofibrillary tangles of tau protein) in the cerebral cortex that have been implicated in the disease. Currently four drugs have been approved but none have shown to significantly treat the symptoms or alter the course of the disease.

Trials are now under way that focus on prevention of the disease in those that are most pre-disposed to developing it. These are people that have the Dominantly Inherited Alzheimer’s Disease or DIAD. Persons with this form of the disease develop amyloid -β plaques in their brains in the 20’s & 30’s. Their children have a 50% chance of inheriting the condition. Study done by Bateman and published in the New England Journal of Medicine, 2012 found that in the DIAD population, they can now track changes in brain pathology, starting many years before symptoms are expected to appear. On a positive note, those with this DIAD mutation have been eagerly enrolling in these and other primary prevention trials targeting amyloid-β.

There is now evidence that Alzheimer’s disease progression is a runaway process after a certain point. The presence of amyloid-β plaques triggers changes in brain metabolism followed by alterations in tau deposition and inflammation. Once the process has started, the tau tangles continue unabated even after removal of amyloid-β plaques. Therefore, Amyloid-β is a prime target for primary prevention.

Jonsson published in Nature, 2012 that a certain population in Iceland with DIAD have a gene mutation that reduces the production of amyloid-β proteins. Treatment is now targeting enzymes involved in the production of these proteins and in clinical trials have reduced production of amyloid-β by much as 80%. Oral drugs that target enzymes such as BACE and gamma secretase are also being developed.

The authors, McDade and Bateman, believes that prevention is the answer. Guidelines for approval of Alzheimer’s drugs are also being relaxed by both the FDA and the European Medicine Agency. A successful outcome will not only enrich the golden years of a significant number of our elderly but also countless other families that support and care for them.

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Alzheimer’s – Prevention May Be the Answer

By 2030, more than 70 million people worldwide are expected to have Alzheimer’s, at a global cost of US $2 trillion. Yet, treatment for this disease has remained as elusive as ever.

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