Ace 08 February 2026

Gregor Johann Mendel: the origin of genetics that today helps us understand dementias

Talking today about genetics, precision medicine or advanced biomedical research is, in reality, talking about a story that began more than 150 years ago in a small garden. There, far from large laboratories and technologies unimaginable in his time, Gregor Johann Mendel laid the foundations of a scientific revolution that continues to shape the course of current research, including in complex diseases such as Alzheimer’s.

A scientist ahead of his time

Mendel was born in 1822 in what is now the Czech Republic and became an Augustinian monk. His life unfolded between teaching, religious life and an uncommon scientific curiosity. At a time when biology was based largely on descriptive observation, he introduced something truly groundbreaking: method, numbers and patience.

For years, in the monastery garden, he crossbred pea plants and recorded with almost obsessive rigor how apparently simple traits—such as flower color or seed shape—were inherited. He was not seeking fame or recognition; he simply wanted to understand how life is transmitted.

The origin of modern genetics

Between 1856 and 1863, Mendel formulated what we now know as the laws of inheritance. His great insight was realizing that traits do not blend in a diffuse way, but are transmitted through discrete units: what we now call genes.

His discoveries went largely unnoticed for decades. It was not until the early 20th century that the scientific community recognized these observations as the true starting point of modern genetics.

From peas to the human genome

Mendel’s legacy goes far beyond botany. His ideas opened the door to understanding that many diseases have a genetic basis and to the development of essential disciplines such as molecular genetics, genomics and personalized medicine.

Thanks to this knowledge, today we can study how specific genetic variations influence the risk of developing neurodegenerative diseases, including Alzheimer’s. These are not genes that “determine” the disease, but pieces of a puzzle that help explain why it appears, how it progresses and why it does not affect everyone in the same way.

Genetics and Alzheimer’s: an integrated perspective

Today, Alzheimer’s research combines genetic, biological and environmental factors. Genetics provides key information to advance early diagnosis and to open new therapeutic avenues.

At Ace, genetic research is one of the fundamental pillars of current knowledge about Alzheimer’s. Since 2005, the center has built a genetic collection of more than 13,000 individuals—the largest in Europe gathered within a single center—which has become a key infrastructure for scientific progress.

Thanks to this sustained effort, we have led projects such as GR@CE, which have made it possible to identify new genes involved in Alzheimer’s disease and to deepen our understanding of the role of the immune system and vascular processes in its development.

This leadership also extends to other neurodegenerative diseases. An international study coordinated by an Ace researcher has, for the first time, identified a new genetic region (NFASC/CNTN2) associated with Progressive Supranuclear Palsy (PSP), a rare neurological disease, opening new pathways for diagnosis and the design of future treatments.

This is work that does not remain confined to the laboratory, but translates into a better understanding of the disease and into real advances in the diagnosis and care of people living with Alzheimer’s.

Gregor Johann Mendel never became aware of the true impact of his work. Nevertheless, every advance in genetics applied to Alzheimer’s is, in a sense, a continuation of that first experiment with pea plants.

Today, this legacy is reflected in knowledge, innovation and commitment—and in the shared conviction that understanding the disease better is the first step toward transforming it. Because the history of science is also the history of people who believe that, one day, Alzheimer’s will be history.