More than 5 million people in the US have Alzheimer’s disease – a major cause of cognitive decline – and this number is expected to almost triple to 16 million by 2050. With figures like these, the race is on to find a cure for the disease. In a new study, a researcher describes a novel, personalized treatment program that he claims has reversed cognitive decline in a small number of patients with memory loss.

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A researcher claims that personalized treatment programs – which involve diet and lifestyle changes – reversed cognitive decline in patients with memory loss.

Dale E. Bredesen, of the Buck Institute Research on Aging in Novato, CA, and the University of California-Los Angeles, published his findings in the journal Aging.

In the US, Alzheimer’s disease is the sixth leading cause of death – killing more people every year than breast cancer and prostate cancer combined.

In a recent spotlight feature discussing whether we are close to finding a cure for Alzheimer’s, Heather Snyder, director of medical and scientific operations at the Alzheimer’s Association, told Medical News Today that Alzheimer’s is the only cause of death in the top 10 that we do not have a way to prevent, stop or slow its progression.

Bredesen supports this claim, adding: “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.”

He notes that combination therapies for other chronic illnesses, such as cancer, cardiovascular disease and human immunodeficiency virus (HIV), have improved outcomes. However, he says such therapies have not been explored in the case of Alzheimer’s, despite there being evidence that the disease may be caused by an array of molecular interactions.

“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,” Bredesen says.

In previous research, Bredesen has strived to better determine the underlying mechanisms of Alzheimer’s.

Past studies have indicated that the disease is caused by sticky plaques in the brain formed by an accumulation of a protein called beta-amyloid in the brain. It is believed these plaques damage and destroy nerve cells, which leads to memory loss.

But Bredesen’s research challenges this theory. He believes that the beta-amyloid protein is part of a bigger set of molecules that contribute to normal brain function, and that an increase in the protein disturbs nerve cell signaling and the balance between the brain’s ability to make or break memories, leading to memory loss.

As such, rather than targeting a single mechanism thought to contribute to Alzheimer’s, he wanted to look at how a combination of therapies worked.

“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,” he explains.

To test his theory, Bredesen enrolled 10 participants to his study. All patients had either Alzheimer’s-related memory loss, amnestic mild cognitive impairment or subjective cognitive impairment.

The plasticity of each patient’s brain – changes in neural pathways and synapses – was analyzed to determine the influence, and each patient underwent a personalized, comprehensive treatment program based on the results.

Fast facts about Alzheimer’s in the US
  • In the US, someone develops Alzheimer’s every 67 seconds
  • 1 in 3 people over the age of 65 die from Alzheimer’s or another form of dementia
  • Of the 5.2 million people with Alzheimer’s, 3.2 million are women.

Learn more about Alzheimer’s

Bredesen discusses one patient as an example – a 67-year-old woman who had experienced 2 years of progressive memory loss.

When reading a book, she would forget what she had read by the time she reached the bottom of the page and would need to start again. She also confused the names of her pets, could not remember numbers and would forget where the light switches were in her home. Because her job involved traveling around the world and preparing analytical reports, she considered quitting.

This patient’s therapeutic program included, but was not limited to:

  • Cutting out all simple carbohydrates from her diet, leading to a 20-pound weight loss
  • Reducing consumption of gluten and processed foods, and increasing consumption of vegetables, fruits and non-farmed fish
  • Fasting for at least 12 hours between dinner and breakfast, and for at least 3 hours between dinner and bedtime
  • Taking up yoga to reduce job-related stress, and meditating for 20 minutes each day
  • Exercising for at least 30 minutes a day, 4-6 days a week
  • Taking melatonin each night (used to ease insomnia), and increasing sleep from 4-5 hours a night to 7-8 hours
  • Taking methylcobalamin (a form of vitamin B), vitamin D3, fish oil and CoQ10 supplements each day
  • Increasing oral hygiene through use of an electric flosser and electric toothbrush, and
  • Reinstating previously discontinued hormone therapy.

In this patient, Bredesen says that after 3 months of following the treatment program, all her symptoms of memory loss had been reversed and are still absent 1.5 years later.

He claims that eight other patients saw reversal of memory loss symptoms within 3-6 months of starting their programs, although one patient with late-stage Alzheimer’s was unaffected by the program.

Commenting on the findings, Bredesen says:

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.

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.”

Bredesen admits that each of the programs are complex, and none of the patients were able to adhere to them at all times. The majority of patients complained about having to take multiple pills each day and making significant diet and lifestyle changes.

He notes, however, that the side effects of the programs are practically non-existent. “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,” he says.

He stresses once more that his findings need to be replicated in larger trials to confirm their effectiveness, as well as identify exactly the extent to which the programs improve memory loss, and how late in the cognitive decline process the programs can be introduced to be effective.

Furthermore, Bredesen says that larger trials should determine whether such programs can be effective in familial Alzheimer’s, and if so, how long these improvements last.

MNT recently reported on a study claiming anxiety, jealousy and moodiness may increase Alzheimer’s risk in women.