Inside Alzheimer's
Friends, has prepared for you a translation of Nature 's wonderful, simple and clear video about what Alzheimer's disease is .
“More than a century ago, the German doctor Alois Alzheimer noticed anomalies in the brain section of a patient with dementia .
Since then, people have begun to study the strange plaques and tangles that he discovered, in the hope that one day we will be able to understand and cure what is now known as Alzheimer's disease.
Plaques are insoluble deposits of the peptide (or protein) amyloid-beta (or A-beta). They are formed when the amyloid precursor protein is sequentially disassembled by two enzymes (or enzymes): beta and gamma secretase. In the process of this analysis, other molecules are also formed that can also contribute to the disease, but A-beta is the main component.
A-beta may incorrectly roll up and become sticky, gradually gluing together with like-like proteins and forming soluble oligomers . However, some of these compounds form long oligomeric fibers that are no longer soluble and are deposited in the brain in the form of plaques.
Oligomers are found in several forms. We do not know exactly which ones are toxic, but studies show that, in one way or another, they weaken the process of signal transmission and plasticity in synapses. Perhaps this is precisely what prevents the formation and retrieval of memories.
Neurons are not the only cells that are affected by Alzheimer's disease. Astrocytes (or stellate neurons) and microglia are also affected.
Microglia are immune cells that cleanse the brain of metabolic products and remove extra synapses during brain development. They also absorb A-beta, but in the process are activated by this protein - the process of releasing inflammatory cytokines , which can damage neurons, is launched. Next, the microglia begins to remove synapses by phagocytosis.
As synapses begin to work intermittently, and neurons die, abnormal patterns of brain activity arise, and soon it can no longer process and store information properly.
Another key aspect of Alzheimer's disease is neurodegeneration . The damage and death of neurons is also triggered by A-beta protein. But some of the effects of its action seem to be controlled by another protein, observed in the brain of patients - the tau protein - an integral part of the coils, which we said at the beginning.
In a healthy neuron, molecules are transmitted along an axon along several “paths” (microtubules), which are ordered using these tau proteins. But in Alzheimer's disease, tau proteins change in such a way that they begin to separate from microtubules, take an unusual shape, and move from the axon to the cell body.
Just like A-beta, tau has many forms, and we also don’t know which ones are involved in the disease. And just like A-beta, these forms either remain soluble, or stick together and form the tangs, which Dr. Alzheimer saw. In a short time, these processes lead to the death of a neuron.
Another problem observed in animal models is that incorrectly folded tau proteins can penetrate healthy neurons through synapses. There, they transform healthy tau proteins into abnormal ones, spreading pathology throughout the brain. The pattern of spread in different areas of the brain corresponds to the symptoms of changes observed from the early to the late stages of the disease. This pattern also reflects how some neurons are more vulnerable to the disease than others.
Despite our progress in understanding Alzheimer's disease, there is no cure. And although drugs are being developed aimed at combating A-beta and tau, it is not known whether they will be effective.
There is only one certainty: supporting basic and clinical research will help us come to successfully diagnosing and curing this devastating disease. ”
“More than a century ago, the German doctor Alois Alzheimer noticed anomalies in the brain section of a patient with dementia .
Since then, people have begun to study the strange plaques and tangles that he discovered, in the hope that one day we will be able to understand and cure what is now known as Alzheimer's disease.
Plaques are insoluble deposits of the peptide (or protein) amyloid-beta (or A-beta). They are formed when the amyloid precursor protein is sequentially disassembled by two enzymes (or enzymes): beta and gamma secretase. In the process of this analysis, other molecules are also formed that can also contribute to the disease, but A-beta is the main component.
A-beta may incorrectly roll up and become sticky, gradually gluing together with like-like proteins and forming soluble oligomers . However, some of these compounds form long oligomeric fibers that are no longer soluble and are deposited in the brain in the form of plaques.
Oligomers are found in several forms. We do not know exactly which ones are toxic, but studies show that, in one way or another, they weaken the process of signal transmission and plasticity in synapses. Perhaps this is precisely what prevents the formation and retrieval of memories.
Neurons are not the only cells that are affected by Alzheimer's disease. Astrocytes (or stellate neurons) and microglia are also affected.
Microglia are immune cells that cleanse the brain of metabolic products and remove extra synapses during brain development. They also absorb A-beta, but in the process are activated by this protein - the process of releasing inflammatory cytokines , which can damage neurons, is launched. Next, the microglia begins to remove synapses by phagocytosis.
As synapses begin to work intermittently, and neurons die, abnormal patterns of brain activity arise, and soon it can no longer process and store information properly.
Another key aspect of Alzheimer's disease is neurodegeneration . The damage and death of neurons is also triggered by A-beta protein. But some of the effects of its action seem to be controlled by another protein, observed in the brain of patients - the tau protein - an integral part of the coils, which we said at the beginning.
In a healthy neuron, molecules are transmitted along an axon along several “paths” (microtubules), which are ordered using these tau proteins. But in Alzheimer's disease, tau proteins change in such a way that they begin to separate from microtubules, take an unusual shape, and move from the axon to the cell body.
Just like A-beta, tau has many forms, and we also don’t know which ones are involved in the disease. And just like A-beta, these forms either remain soluble, or stick together and form the tangs, which Dr. Alzheimer saw. In a short time, these processes lead to the death of a neuron.
Another problem observed in animal models is that incorrectly folded tau proteins can penetrate healthy neurons through synapses. There, they transform healthy tau proteins into abnormal ones, spreading pathology throughout the brain. The pattern of spread in different areas of the brain corresponds to the symptoms of changes observed from the early to the late stages of the disease. This pattern also reflects how some neurons are more vulnerable to the disease than others.
Despite our progress in understanding Alzheimer's disease, there is no cure. And although drugs are being developed aimed at combating A-beta and tau, it is not known whether they will be effective.
There is only one certainty: supporting basic and clinical research will help us come to successfully diagnosing and curing this devastating disease. ”
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