Personalized Treatment Program May Reverse Alzheimer’s Symptoms

Ana de Barros, PhD avatar

by Ana de Barros, PhD |

Share this article:

Share article via email
Personalized Treatment Alzheimer's Symptoms

Personalized Treatment Alzheimer's SymptomsA novel, personalized treatment program with the ability to reverse the cognitive impairment caused by Alzheimer’s disease may have been discovered by a researcher from the Buck Institute Research on Aging, in Novato, California and the University of California-Los Angeles. The findings of the study, which focused on combined therapies rather than finding a cure for the disease alone, were published at the Aging journal.

During his research, Dale E. Bredesen created a personalized treatment program that he believes is able to reverse the process of development of the disease in patients with memory loss.

“In the past decade alone, hundreds of clinical trials have been conducted for Alzheimer’s at an aggregate cost of over a billion dollars, without success,” Bredesen noted, explaining that combined therapies have better results in chronic diseases like cancer, cardiovascular diseases or HIV, but that the personalized treatment approach has not been studied in the case of Alzheimer’s. However, the disease has been proven to be caused by molecular interactions, siliar to other diseases where the personalized treatment approach has worked. “That suggested that a broader-based therapeutics approach, rather than a single drug that aims at a single target, may be feasible and potentially more effective for the treatment of cognitive decline due to Alzheimer’s,” he added.

Prior studies demonstrated that Alzheimer’s is caused by accumulations of the protein beta-amyloid in the brain that lead to the formation of sticky plaques, which are responsible for damaging and destroying nerve cells, as well as for loss of memory. However, Bredesen believes that the beta-amyloid protein is integrated in a larger series of molecules that are part of the normal brain function. Therefore, an increase in the protein damages the nerve cell signaling and the balance between the brain’s ability to make or break memories, causing memory loss.

“Based on the hypothesis that Alzheimer’s disease results from an imbalance in an extensive plasticity network, the therapy should address as many of the network components as possible, with the idea that a combination may create an effect that is more than the sum of the effects of many monotherapeutics,” Bredesen explained, as he believes that combined therapies are more effective than targeting only one mechanism that is thought to be the one responsible for the disease.

During his clinical trials, Bredesen tested his theory on 10 patients who were suffering from Alzheimer’s-related memory loss, amnestic mild cognitive impairment or subjective cognitive impairment, and analyzed the plasticity of their brains, which means variations of the neural pathways and synapses, in order to understand the results of a personalized and comprehensive treatment program.

Nine of the ten patients revealed regressions of their memory loss symptoms, between three and six after the beginning of their treatment programs. However, one of the patients, who suffered from late-stage Alzheimer’s, revealed no reactions to the program. “Results from the 10 patients reported here suggest that memory loss in patients with subjective cognitive impairment, mild cognitive impairment, and at least the early phase of Alzheimer’s disease, may be reversed, and improvement sustained, with the therapeutic program described here,” stated Bredesen.

The researcher admitted, however, that the personalized programs were complex and require that the patients took a large amount of drugs every day, as well as conduct several diet and lifestyle changes. None of the patients were able to adhere to the program at all times. On the other hand, there were no significant side effects reported, and Bredesen noted that, “it is noteworthy that the major side effect of this therapeutic system is improved health and an optimal body mass index, a stark contrast to the side effects of many drugs.”

“This is the first such demonstration. However, at the current time the results are anecdotal, and therefore a more extensive, controlled clinical trial is warranted,” he added, explaining that the findings would need replication in larger studies in order to confirm the effectiveness of the programs and better understand the extent of its effects. In addition, further trials would be needed to understand how late in the disease would it be possible to use the approach, if the programs are effective in familial Alzheimer’s, and the duration of the effects.