Scientists find the genetic secret of Alzheimer’s disease

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In Australia, as the population grows older, we’re hearing more about complex diseases that affect the brain and behavior, like dementia.

Alzheimer’s disease, a type of dementia, is becoming more common. It’s expected that cases of such brain diseases will double in the next 40 years. So, it’s likely that someone you know might be affected by Alzheimer’s.

Alzheimer’s and similar diseases can change the way people think, remember, and solve problems. They also can change how people act or react to things around them.

Understanding these diseases, including how they develop and how to manage them, is not easy.

One big question in studying these diseases is about heritability – how our genes, passed down in families, play a role. The debate is old but still relevant: are our traits determined by our genes or our environment? The answer is both.

Let’s say someone in your family has Alzheimer’s. You might wonder if you will get it too because it’s “in your genes.” The answer is complex.

We are born with certain traits or characteristics, known as phenotypes. For example, having brown eyes is a phenotype, a visible result of your genetic makeup.

Diseases have phenotypes too, like memory loss in Alzheimer’s. Many traits, including disease traits, are influenced by both our genes and our environment. Understanding this influence is crucial for managing and treating diseases.

Understanding Alzheimer’s Heritability

The heritability of Alzheimer’s is estimated to be up to 80%. But this doesn’t mean you have an 80% chance of getting Alzheimer’s if a parent has it. Heritability is about how much a trait varies in a group because of genetics, not about an individual’s risk.

A special case is familial Alzheimer’s, which shows up early in life and has a 50% chance of being passed on to children.

The Challenge of “Missing Heritability”

A big challenge in Alzheimer’s research is “missing heritability.” This is when we know a disease is heritable but can’t find the exact genetic cause.

For simpler diseases, scientists can find genetic variants that cause different traits. But Alzheimer’s is complex; it’s not caused by just one genetic variant. This makes it harder to understand.

Scientists now believe that Alzheimer’s is caused by how different genes interact with each other. There are about 20,000 genes, so the ways they can interact are almost endless. These interactions can influence the traits of Alzheimer’s.

Identifying these interactions helps scientists find genetic “modulators” in Alzheimer’s. These modulators can either decrease or increase the risk of developing the disease, making them important in understanding Alzheimer’s.

Traditional genetic studies aren’t enough to find all these interactions. Without knowing what to look for, these interactions remain hidden, and doctors can’t catch the disease early.

The Role of AI and Machine Learning

Recently, new tools like artificial intelligence (AI) and machine learning are helping scientists study gene interactions more effectively. Tools like VariantSpark are showing how genes relate to each other and affect diseases like Alzheimer’s.

Understanding Alzheimer’s fully means adding the missing pieces of heritability to the puzzle. This helps scientists figure out the causes and early warning signs of the disease. Early identification is key to improving patient outcomes.

Each piece of missing heritability we find gets us closer to better treatments and early intervention strategies.

This research is more than a scientific challenge; it’s about changing lives and creating a future where diseases like Alzheimer’s can be managed more effectively.

If you care about brain health, please read studies about vitamin D deficiency linked to Alzheimer’s and vascular dementia, and blood pressure problem at night may increase Alzheimer’s risk.

For more information about brain health, please see recent studies about antioxidants that could help reduce dementia risk, and epilepsy drug may help treat Alzheimer’s disease.

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