- Donald Weaver
- The Conversation*
As an Alzheimer’s researcher and neurologist caring for people with Alzheimer’s disease, I share the frustration – actually anger – of individuals and families when I tell them that I don’t have a cure to offer.
Over the past year, scientists tackled COVID-19, a previously unknown disease, and within months they developed effective new vaccines.
During that same time period, the list of Alzheimer’s treatment failures grew longer.
Actually, the only drugs approved for the AlzhIt isimer simply relieve some of the symptoms, partially and temporarily, but do not stop the progress of the disease.
Although it was first officially described 115 years ago – although of course it existed long before that – we still do not have a cure for this devastating disease. Why?
Let’s start by following the money. For years, patient advocates have warned of the rising toll and rising costs of Alzheimer’s as the world’s population ages.
Alzheimer’s is severely underfunded compared to cancer, heart disease, HIV / AIDS, and even COVID-19.
Unfortunately, the mistaken belief that Alzheimer’s only affects older people is a contributing factor to this underfunding. However, between 5 and 10% of people with Alzheimer’s are under 65; some are even 40 years old.
Alzheimer’s is also a disease of the whole family, causing anxiety, depression, and burnout in caregivers and loved ones, which generates a disproportionately high socioeconomic cost.
Financing is not the only problem here. The human brain is extremely complex, and Alzheimer’s disease is the most complex in the brain.
The challenges that arise from this confluence of complexities are reflected in the different theories about Alzheimer’s.
The theory more accepted is that the alzhIt isimer is caused by proteins misfolded that aggregate or cluster, killing a brain cells and leading to symptoms of memory loss and reduced cognition.
Initially, the culprit for this misfolding story was a protein called beta-amyloid. More recently, another protein, tau, has emerged as a possible contributor.
Although a wealth of research data has supported this protein misfolding theory, known as the amyloid hypothesis, multiple drugs designed to block the brain’s toxic protein misfolding processes have repeatedly failed in human trials.
In fact, in the past two years, several major clinical trials based on the main hypothesis – that reducing the level of aggregate beta-amyloid that haunts the brains of Alzheimer’s patients would halt the progression of the disease – have failed dramatically. .
But there are many other theories. One is that of neuroinflammation, which suggests that Alzheimer’s arises from an excessive release of toxic inflammatory chemicals from immune cells in the brain called microglia.
The drugs designed on the basis of this theory are fundamentally different from those that address the amyloid hypothesis, and are still in the early stages of the development process.
A different theory states that Alzheimer’s is a disease of the synapses, which are the junctions between brain cells, and another suggests that Alzheimer’s is a disease of the mitochondria, a central structure for energy production in each brain cell.
Challenges to find the cure
The road to a cure will not be easy, and even if these theories lead to drug development, drugs may fail for other reasons.
The alzhIt isimer is a very long chronic disease, probably present for 20 to 30 years before the first symptoms become evident.
Giving a drug when a person becomes symptomatic may be too late to make a difference.
But we don’t have the ability to diagnose it 30 years before the first symptoms, and even if we could, we would have to consider the ethics of administering a potentially toxic long-term drug to someone who may or may not contract a disease in three decades.
Furthermore, unlike the development of antibiotics in which researchers know within days if the drug works, the chronic nature of Alzheimer’s requires long and expensive trials (years of duration) before a response can be obtained.
That time and expense is an additional impediment to drug development.
One last problem is that Alzheimer’s it may not just be a disease. In fact, it can be a set of similar diseases.
A 52-year-old with early-onset / early-onset Alzheimer’s certainly has a distinct and different clinical history than an 82-year-old with late-onset Alzheimer’s.
Will a drug that works for an 82-year-old also work for a 52-year-old? Maybe yes, or maybe no.
Fortunately, despite these many obstacles, a great deal of fascinating and encouraging research is taking place in laboratories around the world.
The science and pharmaceutical industry successes against many other diseases in the last century have often arisen from the gathering of the fruits at hand.
Alzheimer’s is not a ripe fruit, but the apple at the top of the tree, and scientists will have to climb many branches, many of which have never been reached, on the way to a cure.
* Donald Weaver is professor of chemistry and director of the Krembil Research Institute, University Health Network, affiliated with the University of Toronto.
This article was originally published in English on The Conversation and you can read it here.
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Eddie is an Australian news reporter with over 9 years in the industry and has published on Forbes and tech crunch.