Hypervigilance and fear are the most common reactions of people who have a parent (or another family member) affected by Alzheimer’s disease. Although a family history of Alzheimer’s increases the risk of developing the disease, the picture of risk factors proves to be much more complex, just like that of prevention.

Writer Carol Berkower recalls the day her 64-year-old mother told her she had been diagnosed with Alzheimer’s. It was 30 years prior to writing, when Berkower was only 20 years old, but the shock experienced then was amplified by the fear that, one day, she might receive the same diagnosis. Five years later, after the disease had robbed her of even her ability to speak, the mother died, and her daughter was already beginning to identify what she thought might be the first signs of early dementia. Trying to calm her fear, Berkower decided to get on with her life until the 50-year mark, hoping that in the following two decades scientists would be able to find the long-awaited cure.

Marriage, two children, a career, a doctorate, and the decision to emigrate followed. Twenty years passed quickly, and at the end of them, Berkower would face the questions that torment many children whose parents have been diagnosed with Alzheimer’s: how big is the risk of being afflicted with the same disease? And how effective are the treatment options today, compared to those available in our parents’ time?

What we do and don’t know about Alzheimer’s disease

“We are entering a golden age of Alzheimer’s research.” This is the message that Keith Fargo, the director of scientific programs and outreach for the Alzheimer’s Association, conveys to those disappointed by the fact that, after decades of research, there are still many aspects that researchers have not elucidated.

There is no cure for the disease (there are, however, drugs that can relieve symptoms but there aren’t any to at least slow down the process of neuron destruction), the complex genetic processes behind the disease have not been discovered, and the elements that trigger the condition have yet to be established with certainty.

Globally, every 3 seconds, a person is diagnosed with dementia. In 2020, there were more than 55 million people who had developed some form of dementia (60-70 per cent of them have Alzheimer’s disease), and experts estimate that this number will double every 20 years.

Although Alzheimer’s is the most common type of dementia, the etiopathogenesis of the disease is not fully known. So far, two proteins associated with neurodegeneration have been studied: beta-amyloid proteins (which, as the disease progresses, build up, forming amyloid plaques that obstruct communication between neurons) and tau proteins, which cause “tangles” in the brain tissue, interrupting the functioning of neurons and thus causing their death.

A 2021 study, the first to analyse data obtained from research on human subjects, disproves the theory that protein plaques form in one area and then spread to other cortical regions.

Although Alzheimer’s disease was thought to develop in a similar manner to many types of cancer, research has shown that at the onset of the disease, there are already protein build-ups in several regions of the brain, which is why trying to deter their spread will not succeed in slowing the progression of the disease, says researcher Georg Meisl, the study’s coordinator.

The researchers found that the number of protein deposits doubled only after five years, showing that neurons have the ability to fight off the protein build-up—good news for scientists looking for treatments that could boost neurons’ ability to stop protein accumulation, thereby delaying progression to severe forms of the disease.

Infections: a cause of Alzheimer’s disease?

In recent years, a series of experiments and clinical data have outlined and supported the hypothesis of an infectious pathogenesis of Alzheimer’s disease.

In 2017, the public benefit corporation Alzheimer’s Germ Quest, Inc launched the $1 million Challenge Award, a prize that was to be offered over the following three years to anyone who could prove that a specific infectious agent causes Alzheimer’s.

Dr Leslie Norins, the founder of the corporation, stated that “it appeared that many of the reported characteristics of Alzheimer’s disease were compatible with an infectious process.” After reviewing the evidence in the medical literature, Norins concluded that a germ, “identity not yet specified, and possibly not yet discovered,” which he calls the “Alzheimer’s germ,” is responsible for most Alzheimer’s cases.

Among the studies that support his beliefs, Norins cites two that were published in 2010: a study that found the Alzheimer’s death rate among U.S. neurosurgeons to be nearly two and a half times higher than the general population, and another that showed that people whose partners suffer from dementia have a 1.6 times greater risk of developing the disease.

In the end, no one won the million dollars, but eight researchers split $200,000 of this prize after providing plausible evidence of six pathogens that could play a role in causing the disease. However, none of them provided evidence that persuaded Norins of a single “Alzheimer’s germ.”

Commenting on the results, he says that it is possible that there is not a single “Alzheimer’s germ,” but several (be they bacteria, viruses, fungi or parasites). There is also the possibility that our brain is like a train station for germs, with a saboteur hiding among the passengers. It could have escaped the attention of researchers, says Norins, recalling how late the bacterium Helicobacter pylori was identified as a cause of the gastric ulcer.

Even though the hypothesis that Alzheimer’s disease is an infection of the brain seems revolutionary, it is not, in fact, new. More than a century ago, psychiatrist Oskar Fischer suggested that beta-amyloid plaques were caused by a brain infection, and his studies were discovered in 2008 in historical archives in Prague (Fischer died in the Theresienstadt concentration camp, in 1942).

Commenting on studies showing a possible association between the herpes virus and Alzheimer’s disease, Alzheimer’s specialist Sam Gandy says these findings could open the door to new treatment options for a disease “where we’ve had hundreds of failed trials” and that this information does not change the existing data about the risk we have of developing the disease.

Genetics and Alzheimer’s disease

In 2022, a landmark study into the genetic factors of Alzheimer’s disease was published, representing the culmination of 30 years of research, as Professor Julie William stated.

The study’s researchers, who analysed the genomes of more than 100,000 Alzheimer’s patients and compared them with the genomes of more than 600,000 healthy subjects, identified 75 genes linked to a higher risk of developing Alzheimer’s disease, 42 of which were newly discovered. In addition, the study also found evidence to support the role of inflammation and the immune system in the development of the disease.

The study opens new avenues in terms of therapeutic intervention and the development of algorithms to predict whether a person will be affected by this disease throughout their life, says Rebecca Sims, one of the authors of the study.

This is good news for those who have had parents or relatives affected by Alzheimer’s. However, until this information can be put to fruition, what should those who have seen a close-up of the monstrous face of Alzheimer’s disease know and, more importantly, do?

Family history and the risk of developing Alzheimer’s

Wanting to better understand the condition her mother had suffered from, and especially the risk of developing the disease herself, Carol Berkower sought out Richard Mayeux, the researcher who had diagnosed her mother 30 years earlier. Mayeux had become the co-founder of an Alzheimer’s research institute, and while he had not been able to find a cure for the disease, he discovered many things about how it is passed down through generations.

Mayeux assesses relatives of Alzheimer’s patients who are afraid of developing the disease themselves. He conducts a baseline evaluation of their mental function, testing their ability to do maths, remember a story or a few words, or relate current information. The patients return to his office for yearly follow-ups, until they are convinced they aren’t progressing, and “then they send me a postcard saying, ‘I’m still good, doc.’”

In 2019, a group of researchers analysed data from more than 270,000 death certificates in Utah to measure a person’s risk of developing Alzheimer’s.

Unlike other studies, this one showed that the disease of second and even third-degree relatives also influences the individual risk of developing the condition, says Professor Keoni Kauwe.

The researchers found that people with one first-degree relative with Alzheimer’s disease (parents and siblings who shared both parents) had a 73 per cent increased risk of developing the disease (the odds of developing the disease increased with the number of first-degree relatives with Alzheimer’s). For those with three third-degree relatives, this risk is 43 per cent. The lowest risk of the disease was recorded in people who had no relatives with Alzheimer’s or only one or two third-degree relatives diagnosed with this form of dementia.

Even though people who have close relatives with Alzheimer’s often become hypervigilant about any symptoms that might betray their own disease, we shouldn’t overestimate that risk, concludes an analysis that shows many doctors are against genetic testing—this is not the best predictor of a late-onset Alzheimer’s diagnosis—and believe that most people with a family history of Alzheimer’s will not develop the disease after all.

There is a small number of cases (1-2 per cent of the population) in which genetics play an important role—children of individuals who had an early onset of the disease (currently, three forms of early onset Alzheimer’s are recognized, caused by mutations in one of the APP, PSEN1 or PSEN2 genes) have a 50 per cent risk of inheriting these faulty genes and developing the disease.

The strongest risk factor for dementia, however, remains age, even though dementia is not a normal part of the ageing process. The risk increases with age: after the age of 65, the risk of the disease doubles every 5 years. One in 20 Canadians over the age of 65 and 1 in 4 Canadians in the 85+ age category has Alzheimer’s.

This disabling disease is most likely a combination of genetic, environmental, and lifestyle factors, says Riddhi Patira, an assistant professor of neurology at the University of Pittsburgh Alzheimer’s Disease Research Centre. “Any cause [you] can imagine, you will find a study about it in the literature. Everything is hot in Alzheimer’s research because people are really desperate” for a cure, points out Patira.

Those who notice that they have memory loss should go to the doctor to be evaluated only if the changes are persistent, have occurred for several months, and have been noticed by other family members, says researcher Frank Jessen.

Can Alzheimer’s be prevented?

A medical evaluation can loosen the grip of fear, especially since some symptoms of Alzheimer’s disease are similar to those of treatable diseases, from thyroid problems to urinary tract infections. “Anxiety itself can affect memory, with forgetfulness stoking yet more anxiety,” says neurology professor David Wolk. People who turn their fear into a positive factor are those who make lifestyle changes and reap the benefits, says Wolk.

In fact, after 2010, research began to bring more and more evidence that the onset of Alzheimer’s disease could be influenced by lifestyle, amid a reluctance of the scientific community to accept this idea.

Thus, the authors of a 2017 study estimated that 35 per cent of dementia causes can be attributed to potentially controllable factors, and a 2013 study showed that people with a Mediterranean diet scored best on cognitive tests. A heart-healthy diet is also friendly to our brain, concluded another study that highlighted the fact that a plant-based (especially leafy green vegetables), whole-grain diet is associated with a reduced risk of Alzheimer’s disease.

Frequent consumption of foods rich in flavonols (antioxidants found predominantly in fruits, vegetables, and tea) reduces the risk of Alzheimer’s in the elderly, according to researchers at Rush University in Chicago. On the other hand, frequent consumption of processed foods increases the risk of Alzheimer’s disease or senile dementia by 52-74 per cent.

Studies that have tried to determine whether a particular food or nutrient influences brain health have come up with conflicting results, leading to the idea that one should integrate as many healthy foods as possible into the diet, rather than looking for a single beneficial food, says Leon Flicker, from the University of Western Australia.

Regular physical activity is the recommendation that researcher Richard Mayeux offers to people who want to reduce the risk of developing Alzheimer’s. The suggestion is based on a long line of studies that have shown that exercise offers benefits even in the early stages of the disease.

Maintaining cognitive activity throughout life is another element of preventing brain decline, according to specialists. An intellectually and socially active lifestyle protects the brain, according to a 2022 study that looked at factors that may contribute to creating a “cognitive reserve” that could act as a buffer against the onset of dementia.

The level of education, occupation, ability to read, participation in religious activities within a group, or leisure activities are among the factors that influence this reserve. Evidence provided by the researchers suggests that continuous learning protects the brain even in people who scored low on cognitive tests in childhood.

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Worrying about what we might lose in the future could divert our attention not only from the things we enjoy now, but also from the choices we can make to prevent (or at least try to prevent) a neurodegenerative disease for which medicine does not yet offer viable treatment options. Postponing lifestyle adjustment is just another misstep in enhancing our increasingly fragile well-being.

If it is true that the biological processes that cause mental decline begin a decade or even two before the first symptoms set in, it is never too early to make choices that keep us as far away from the disease that “doesn’t care who you are,…who you used to be or even who you might have become,” and about who knows how many other things.

Carmen Lăiu is an editor at Signs of the Times Romania and ST Network.