Why is there no cure for Alzheimer’s disease?

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This article was originally published in The Conversation, an independent, non-profit source of news, analysis and commentary from academic experts. Disclosure information is available on the original site.

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Author: Donald Weaver, Professor of Chemistry, Director, Clenville Institute, University of Toronto University Health Network

As a researcher studying Alzheimer’s disease and a neurologist who cares for people with Alzheimer’s disease, I share the frustration and certainly anger of people and families when I say there is no cure.

Over the past year, scientists have tackled a previously unknown disease, COVID-19, and within a few months have developed a new vaccine that is effective. In that same time frame, the list of treatment failures for Alzheimer’s disease grew longer. Currently, the only drug approved for Alzheimer’s disease is to partially and temporarily relieve some of the symptoms, but it does not stop the disease from progressing.

It was first officially described 115 years ago, and of course existed long before that, but we still don’t have a cure for this catastrophic disease. why?

Let’s start by following the money. For years, patient advocates have pointed out that as the world’s population ages, Alzheimer’s disease prices rise and costs rise. Alzheimer’s disease is significantly underfunded compared to cancer, heart disease, HIV / AIDS, and even COVID-19.

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Sadly, the false belief that Alzheimer’s disease affects only the elderly contributes to this lack of funding. However, 5-10% of people with Alzheimer’s disease are under the age of 65. Some people are in their 40s. Alzheimer’s disease is also a family illness that causes anxiety, depression and malaise in caregivers and loved ones, forcing disproportionately high socio-economic costs.

Contradictory theory

Financing is not the only issue here. The human brain is very complex, and Alzheimer’s disease is the most complex disease in the brain. The challenges that arise from this conflict of complexity are reflected in many competing theories of Alzheimer’s disease.

The oldest theory is that Alzheimer’s disease is caused by accidentally folded proteins that aggregate or aggregate, killing brain cells and causing symptoms of amnesia and cognitive decline. Initially, the culprit in this false folding story was a protein called beta-amyloid. Recently, another protein, tau, may have contributed.

The false folding theory of this protein, called the amyloid hypothesis, is supported by extensive research data, but several drugs designed to block the false folding process of toxic proteins in the brain have been tested in humans. It has failed repeatedly. In fact, in the last two years, several major clinical trials based on the main hypothesis in the field that lowering the level of aggregated beta-amyloid that riddles the brain of patients with Alzheimer’s disease stops the disease from progressing dramatically Did.

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And there are many other theories. A new heavyweight candidate is the neuroinflammation theory of Alzheimer’s disease, suggesting that the disease results from the over-release of toxic inflammatory chemicals from immune cells in the brain called microglia. Drugs designed to address this theory are fundamentally different from drugs designed to address the amyloid hypothesis and are still in the early stages of development.

Another theory claims that Alzheimer’s disease is a disease of synapses that are connections between brain cells, and yet another theory is that Alzheimer’s disease is the central structure of energy production in all brain cells, mitochondrial disease. It suggests that it is ill.

Challenges in finding a cure

The path to treatment is not easy, and even if these theories lead to drug development, these drugs can fail for many other reasons.

Alzheimer’s disease is a very long and chronic illness that probably develops 20 to 30 years before the first symptoms become apparent. It may be too late to administer the drug when a person shows symptoms and cannot make a difference. However, it cannot be diagnosed 30 years before the first symptom. Even if you can, you need to consider the ethics of giving potentially toxic drugs to those who may or may not get sick in the long run. 30 years.

Also, unlike the development of antibiotics, where researchers know if a drug works within a few days, the chronic nature of Alzheimer’s disease requires long and costly trials to get an answer. .. Such time and money are a further obstacle to drug development.

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One of the last problems is that Alzheimer’s disease may not be just one disease. It may actually be a collection of similar illnesses. The 52-year-old with early-onset Alzheimer’s disease does have a different clinical course than the 82-year-old with late-onset Alzheimer’s disease. Do drugs that work at the age of 82 work for the illness of a 52-year-old person? Maybe, or maybe not.

Thankfully, despite many of these hurdles, laboratories around the world are doing a lot of fascinating and encouraging research. The success of the science and pharmaceutical industry against many other illnesses over the past century has often stemmed from choosing hanging fruits. Alzheimer’s disease is not a hanging fruit, but an apple at the top of the tree, and scientists have to climb many branches on their way to treatment. But we get there.

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Donald Weaver is funded by the Canadian Institute of Health, the Clenville Foundation, the Weston Brain Institute, and the Harrington Discovery Institute.

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This article has been republished by The Conversation under a Creative Commons license. Disclosure information is available on the original site. Read the original article:

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