What happens in my brain when I have Alzheimer’s disease?

Unfortunately, we are used to hearing about different types of dementia, but they generally do not explain clearly what happens to the brain in these cases, so the purpose of this article is to explain, in the simplest way possible, what happens to the brain. diagnosed with Alzheimer’s disease.

In addition, I will include one of the most recent and encouraging advances in the treatment of Alzheimer’s disease. This breakthrough, which was recently published in the journal Nature, is so important that its findings can change the course of the disease as we know it. .

  • In Alzheimer’s disease.
  • There is terrible degeneration of the brain.
  • Mainly in the hippocampus.
  • Entorrinal cortex.
  • Neocortex.
  • Basal nucleus.
  • Locus coeruleus and rafe nuclei.

But what’s all this? There are different areas of the brain involved in learning formation, memory and emotional balance, and as you can see, these functions are greatly affected in patients with Alzheimer’s disease.

And how do these areas degenerate? With the development of amyloid or amyloid plaques and neurofibrillal balls, but before explaining what these plaques and balls are, we need to know how neurons form:

Amyloid plaques are deposits located outside brain cells composed of a nucleus whose protein is called beta-amyloid, these deposits are surrounded by axons and dendrites in the process of degeneration, this degeneration process is natural in any human brain, it is not pathological.

In addition, there are activated microglyocytes and reactive astrocytes, which are cells involved in the destruction of damaged cells, also called phagocytic neuroglyocytes, which are responsible for the destruction of degenerated axons and dendrites, leaving only a beta-amyloid nucleus.

Neurofibrillary balls are made up of extinguishing neurons that contain intracellular accumulations of interlaced tau protein filaments. Normal tau protein is a component of microtubules that provide the cellular transport mechanism.

During the course of Alzheimer’s disease, an excessive amount of phosphate ions adhere to the strands of the tau protein, thus altering its molecular structure, which becomes a series of abnormal filaments observed in the soma and dendrites closest to the cells of the cerebral cortex. .

Ions that, on the other hand, modify the transport of substances within the cell, so that it dies, leaving behind a tangle of protein filaments.

Wait, did you just say the neurons are degenerating? Yes and this is something that occurs in normal aging, but in the case of Alzheimer’s disease, amyloid plaque formation occurs due to the production of a defective form of beta-amyloid, which causes the onset of neurological death, differentiating it from normal old age.

That is, in the plasticity that we all have in the brain, in which there are neurons that degenerate but do not cause any damage or are replaced by others without noticeing their absence, there is a change in this process caused by beta plates. Amyloid.

The journal Nature recently published an article entitled “Alzheimer’s Disease”: Amyloid Attack?Protein? (Alzheimer’s disease: attack on beta-amyloid protein), whose main author is Eric M. Reiman. This article details the discovery of new advances in the treatment of Alzheimer’s disease, especially beta-amyloid protein.

What Reiman has been looking for is a new drug that prevents the destruction of neurons and the accumulation of amyloid protein plaques, which, as we explained above, is considered one of the main causes of cognitive decline in Alzheimer’s disease.

Felix Viauela, neurologist and researcher at Virgem Macarena Hospital, says that “this drug reaches the brain, adds to the deposit of this toxic substance and eliminates it”. In addition, “we have shown that the higher the amount of new drug administered, the higher the recovery of patients. “

But the researchers themselves point out that, for the time being, this is research being conducted in 300 hospitals in the United States, Europe and Asia, mainly in patients with mild cognitive impairment (DCL). While it is a very encouraging development, there is still a long way to go before it can be implemented and its long-term effects can be demonstrated.

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