A Different Role for Beta Amyloid Protein?

Adapted from an article by Dr. Michael Jurgelewicz titled “Alzheimer’s Disease Amyloid Hypothesis Crumbling”

The presence of amyloid protein in the brains of Alzheimer’s patients has for many years been at the core of scientific research. Developing medication targeting the removal of amyloid proteins and plaques has therefore been the focus of pharmaceutical companies. However, several promising drug trials have been stopped due to subjects in the treatment group faring so much worse than those in the placebo group. And now, another drug called Solanezumab, which was intended to reduce the aggregation of beta-amyloid proteins has proven to be a disappointment. Interestingly, new findings now show that these proteins are likely protective, and are a response to inflammation in the brain

While the aggregation of these protein fragments into insoluble plaques no doubt interferes with synaptic transmission, its presence is often not seen in significant amounts until later in the disease progression. As importantly, there are Alzheimer’s patients who do not exhibit significant plaque deposits, and there are individuals who do show amyloid plaque build-up but are not suffering from dementia.

According to Dale Bredesen, MD, who has designed a multi-pronged diet and lifestyle protocol that has been shown to reverse Alzheimer’s and its precursor, mild cognitive impairment (MCI), in a small but extremely promising study, “The production of the amyloid is a protective response. The idea of just getting rid of the amyloid without understanding why it’s there actually makes very little biological sense.” Other researchers agree and suggest that amyloid is a key regulator of brain homeostasis. During AD, even though amyloid protein accumulates in the brain, it does not contribute to its primary pathogenesis. From this perspective, it follows that developing successful alternative therapies for AD will be slow until closer attention is paid to understanding the underlying physiological causes of dementia and the function of the amyloid protein.

If amyloid proteins are, in fact, a protective mechanism, then it makes sense that drugs intended to prevent the formation of these proteins have either had no impact on disease progression or, as the case has been, have actually caused the disease to worsen. Research dollars would be better spent pursuing avenues that are more promising, such as metabolic therapies involving ketone-based brain fuel metabolism. Some researchers are shifting from the amyloid focus to a mitochondrial hypothesis, wherein mitochondrial dysfunction—and the resulting disruption of cellular energy production—is believed to be the driving factor in the cognitive decline.

Adapted from an article by Dr. Michael Jurgelewicz titled “Alzheimer’s Disease Amyloid Hypothesis Crumbling”

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