
To remember a name, follow a conversation, or learn something new, our brain needs energy. One of its main sources is glucose, which the brain uses to support its functions.
The way the brain processes and uses glucose has been a major area of research into Alzheimer's disease for years. Studies have shown that changes in energy metabolism can occur during the development of the disease, raising questions about the role that insulin may play in brain function.
This research has also given rise to the term “type 3 diabetes.” It is used by some researchers to describe the possibility that the brain develops a type of insulin resistance, which may be linked to nerve cell damage and memory problems.
However, it is important to note that “type 3 diabetes” is not an officially recognized form of diabetes nor a separate diagnosis of Alzheimer's.
What role does insulin play in the brain?
Insulin is usually associated with regulating blood sugar levels. But its action is not limited to this process. In the brain, it participates in mechanisms that support communication between nerve cells, learning, and memory.
When cells become less responsive to insulin signals, this condition is known as insulin resistance. Researchers are investigating whether and how this phenomenon might affect the brain's use of energy and the functioning of neurons.
However, the connection is more complex than the idea that the brain simply “runs out of fuel.” Most of the glucose the brain uses enters the cells without the need for the direct action of insulin.
For this reason, research also focuses on how nerve cells respond to insulin signals and whether changes in these processes can affect the maintenance of their functions.
What do studies show about the link between Alzheimer's and insulin?
Several studies have found a link between type 2 diabetes and a higher risk of developing dementia, including Alzheimer's disease.
Also, analyses of brain tissue from people who have suffered from Alzheimer's have shown signs of reduced insulin response, even in cases where the people did not have a diagnosis of diabetes.
A review of studies published in the scientific journal Diabetology & Metabolic Syndrome examines these connections and treats insulin resistance as a possible mechanism that links metabolic disorders with the damaging processes observed in Alzheimer's.
Other biological mechanisms may also be involved in this process, such as inflammation and the accumulation of certain proteins in the brain.
However, this data does not prove that insulin resistance is a direct cause of Alzheimer's. It does point to a link that requires further study to fully understand.
Why is the term "type 3 diabetes" controversial?
Alzheimer's is a complex disease, the development of which is influenced by age, genetic predisposition and various biological mechanisms.
The use of the term "type 3 diabetes" may create the impression that there is a single explanation for the disease, while the scientific reality is much more complex.
Researchers are still trying to answer some fundamental questions:
Do disorders in insulin action appear before the development of Alzheimer's?
Can they accelerate the progression of the disease?
Or are they, at least in part, a consequence of damage already occurring in the brain?
Does the importance of these mechanisms vary from one patient to another?
So far, scientific evidence does not provide definitive answers to these questions.
Does diabetes mean a person will develop Alzheimer's?
No. Having type 2 diabetes does not mean that a person will definitely develop Alzheimer's. The disease can also occur in people who do not have diabetes.
Keeping your blood sugar levels under control is important for overall health and can help manage some risk factors related to brain health. However, it does not guarantee prevention of dementia or Alzheimer's.
For this reason, the term "type 3 diabetes" should be understood as a research hypothesis and not as a diagnosis that can be given to a person based solely on memory problems or the presence of diabetes.