A Progress Report on the Search for a Cure for Alzheimer’s Disease

Oct 26, 2022

Followers of Everything Retirement know that we cover the issue of Alzheimer’s disease and other dementia-related conditions with considerable frequency.

It’s a vitally important issue in the ageing process and one that you, our readers, tell us is of huge significance to you.

Scientists around the world have continued to chip away at the genetic underpinning of this heartbreaking disease that steals the mind, leaving the body empty of its former self.

Genetic Foundations

Believe it or not there are a total of 75 genes – and counting – connected to the development of Alzheimer’s. This year, 2022, a new gene called MGMT was identified, and this one might explain why women are two-thirds more likely to be diagnosed with Alzheimer’s than men.

Pathways to Alzheimer’s

With so many genes contributing to the development of Alzheimer’s and other types of dementia, scientists are increasingly convinced that each person’s journey may be different.

A recent edition of Nursing Times reported: “Once you have seen one person with Alzheimer’s, you’ve seen one person with Alzheimer’s,” a bleak but true verdict on what is known technically as a multifactorial disease.

Translated, this means that the disease is made up of different pathologies, and each person has their own road. The disease presents differently and progresses differently in different people.

One key genetic pathway is APOE ε4, a gene variant responsible for encoding proteins that carry cholesterol in the brain.

Having one copy of the gene puts people over the age of 65 in danger, while having two copies is considered the strongest risk factor for the future development of Alzheimer’s in that age group.

Another pathway to Alzheimer’s is inflammation, which most seniors suffer from in one form or another.

According to Science Daily: “Neuroinflammation, or inflammation in the brain, has emerged as an important line of inquiry in Alzheimer’s disease research.”

The Role of Amyloid Plaque

A recent report on CNN about Alzheimer’s quoted neurologist Professor Rudy Tanzi, who works at the MassGeneral Institute for Neurodegenerative Disease:

‘Many people may not know this, but after 40 years old, just about all of us start to build up the initiating pathology of Alzheimer’s, which is amyloid plaque in the brain and the neurofibrillary tangles. It’s part of life, just like most of us begin to build up a little bit of plaque in our arteries from cholesterol.’

The CNN story went on to state: “Dr. Tanzi estimates some 30 million to 40 million Americans have enough amyloid in their brains right now to benefit from a drug to lower it – if science had the ability to do so safely and affordably.

‘I like to say the amyloid is like the match, and the tangles are like brush fires that propagate and spread over decades,’ Professor Tanzi was quoted as saying. ‘And along the way you’re triggering big forest fires, that’s neuroinflammation.’

By the time a person shows any signs of cognitive decline, he added, ‘the forest fire of neuroinflammation is blazing,’ and it’s too late to rescue the brain significantly and improve thinking and memory skills.”

Prevention is Cure

Apart from medical research designed to identify the roots of Alzheimer’s, a factor of massive importance is prevention.

Preventive methods are a key focus of much of today’s research.

Lifestyle changes such as improving exercise, eating a plant-based diet, addressing sleep deficits, reducing stress, and engaging in activities that promote cognitive vitality are crucial to brain health.

As is keeping cholesterol and blood sugar in check.

The prevention narrative, driven by important lifestyle changes, is one we at Everything Retirement have been advocating for the past several years, and it’s based on science – not guesswork.

A cure for Alzheimer’s may be a distant dream, but prevention is a strategy we can take ownership of now. It’s not a guarantee against dementia, but with evidence to suggest it helps, we’re keen to adopt it.



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