About 50 million people around the world livewith Alzheimer's disease. And as the population ages in many countries, the numbers suffering from this disease are steadily growing. We know that Alzheimer's is caused by problems in the brain. Cells begin to lose their functions and eventually die, which leads to memory loss, decreased cognitive abilities and even serious changes in personality. Certain areas of the brain also narrow during the process of atrophy, which leads to a significant loss in brain volume. But what exactly is going on in the brain?
The main way the disease spreadsthrough a violation of the connection between neurons, especially cells that process and transmit electrical and chemical bonds between brain regions. This leads to the death of brain cells and, as we think, to the accumulation of two types of protein, amyloid and tau. The exact interaction between the two proteins is largely unknown, but amyloid accumulates in sticky clusters known as amyloid beta plaques, while tau accumulates inside dying cells known as neurofibrillary tangles.
One of the difficulties in diagnosing a diseaseAlzheimer's is that we do not have a reliable and accurate way to measure these protein accumulations in the early stages of the disease. In fact, we cannot definitively diagnose Alzheimer's disease until the patient dies by examining the actual brain tissue.
Another problem is thatamyloid beta plaques can also be found in the brains of healthy patients. This suggests that the presence of amyloid and tau proteins cannot explain the entire history of this disease.
Later studies show thatchronic inflammation may play a role. Inflammation is part of the body’s system of protection against disease, which manifests itself when white blood cells secrete chemicals to protect the body from foreign substances. But over a sufficiently long period of time, it can also cause damage.
Long-term tissue damage in the braininflammation can be caused by the accumulation of cells known as microglia. In a healthy brain, these cells absorb and destroy waste and toxins. But in patients with Alzheimer's, microglia cannot clear this garbage, including toxic tangles of tau or amyloid plaques. The body activates more microglia in an attempt to clear this debris, which in turn leads to inflammation. Long-term or chronic inflammation gradually damages brain cells and ultimately leads to their death.
Recently, scientists have identified a gene calledTREM2, which may be responsible for this problem. Typically, TREM2 directs microglia to cleanse amyloid beta plaques in the brain and helps fight inflammation in the brain. But scientists found that the brains of patients whose TREM2 gene does not work correctly accumulate amyloid beta plaques between neurons.
Many Alzheimer's patients also experienceheart and circulatory problems. Amyloid beta deposits in the arteries of the brain, atherosclerosis (hardening of the arteries), and microstrokes can also play a role.
Vascular problems can further reduceblood flow in the brain and break down the blood-brain barrier, a structure that is important for removing toxic waste from the brain. It can also prevent the brain from absorbing all the necessary glucose - some studies have suggested that this can happen before toxic proteins associated with Alzheimer's disease appear in the brain.
Scientists are penetrating deeper into the brain, in particular inexact connections between neurons, known as synapses. A recent study published in Nature describes a process in cells that can help break down these synaptic connections between neurons. The findings show that it can occur when a specific synaptic protein (known as RBFOX1) is missing.
Thanks to this kind of research, nowMany new drugs have appeared that are being tested and developed to eliminate one or more changes in the brain that occur in Alzheimer's disease. Many researchers believe that a more personalized approach to Alzheimer's patients is the future.