News of health, medicine and longevity. Amyloid plaques, characteristic of Alzheimer's disease, are detected already in youth Substances that dissolve amyloid plaques

Only the lazy have not heard about “bad” cholesterol. Everyone knows that it can be deposited on the walls of blood vessels and lead to various diseases that cholesterol can cause a stroke or heart attack. Therefore, upon reaching conscious adulthood, many people wonder how to cleanse blood vessels from atherosclerotic plaques in order to avoid these consequences. Let's talk about this from the point of view of not traditional, but official medicine.

What are cholesterol plaques

Each human organ receives nutrition from vessels, of which there is a huge and extensive network in the body. Blood flowing through the vessels is not a solution, but a suspension, when a suspension of cells, called formed elements, floats in the liquid. The liquid part of the blood does not at all resemble water, which is explained by the molecules dissolved in it, mainly of a protein nature. But they also “float” in the blood various products fat metabolism, in particular cholesterol, triglycerides, lipoproteins.

According to the laws of physics, blood moves through the vessels in such a way that a “trickle” flows in the center, practically free of cells, and most of the formed elements “go” along the edges, representing a kind of “quick response department”: in response to damage to the vessels, they immediately descend from here platelets, “closing” the gap.

The liquid part of the blood also comes into contact with the vascular walls. As we remember, the products of fat metabolism are dissolved in it. There are several different ones, cholesterol is only one of the components. This system is structured as follows: normally, “bad” fats are in balance with their antagonists, “good” fats (“good” cholesterol). When this balance is disturbed - either the number of “bad” ones increases, or the volume of “good” ones decreases - fatty tubercles - plaques - begin to be deposited on the walls of arterial vessels. The risk of depositing such plaques is judged by the ratio of good fats (they are called “high-density lipoproteins” - HDL) and the sum of low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL). This can be done using a blood test from a vein, called a lipid profile.

Such a plaque is dangerous in the following ways:

• It can come off and, having passed with the blood flow to a vessel of a “suitable” diameter, clogs it, thereby depriving the area feeding from there of some kind of nutritional organ. The smaller the vessel, the smaller the area that dies, the less the functioning of this organ and the body as a whole is disrupted (there is “duplication” within the tissue of each organ, thanks to which each “piece” receives nutrition from several small-diameter vessels at once).
• The blood is forced to bypass the plaque, as a result of which, instead of a uniform flow in the vessel, “vortices” are created when part of the blood flowing near the wall covered with the plaque has to return back. Turbulence in the blood flow impairs the nutrition of the blood supply to the organ. Here the relationship is the same as in the point above: the larger the diameter of the artery damaged by the plaque, the more the organ suffers.
• If the composition of the blood does not change, and the amount of HDL and enzymes that should “break off” the plaque does not increase, the body tries to limit it. To do this, he sends to the place of plaque deposition immune cells, whose task is to “bite off” pieces of plaque and digest them. But the cells are unable to do this: instead of digesting, the immune cells are damaged by cholesterol and fats, and remain “lying” around the cholesterol. Then the body decides to cover this formation connective tissue, and the plaque increases in size even more, now worsening the blood supply to the organ not only due to turbulence, but due to a decrease in the lumen of the vessel.
• Covering with connective tissue is good for the plaque and bad for the vessel. Now, if something damages the plaque, it will “call” platelets to itself, which will form a blood clot on its surface. This phenomenon, firstly, will further reduce the diameter of the vessel, and secondly, it will increase the risk (especially in vessels with “active” blood flow) of a blood clot breaking off and blocking a smaller vessel.
• A long-existing plaque becomes covered with calcium salts. Such a wall formation is already stable and will not come off without intervention. But it tends to grow and reduce the lumen of the vessel.

The rate of plaque formation is affected by:

• consumption of animal fats;
• smoking;
• diabetes;
• excess weight;
• physical inactivity;
• high blood pressure;
• binge eating;
• eating large amounts of simple carbohydrates with food.

The localization of plaque deposition is unpredictable: it can be either the arteries supplying the brain or the arteries of the kidneys, limbs or other organs. Depending on this, they can cause:

• ischemic stroke;
• angina pectoris;
• myocardial infarction;
• intestinal gangrene;
• aortic aneurysm;
• dyscirculatory encephalopathy, which is manifested by memory deterioration, headaches, decreased ability to analyze what is happening;
• deterioration of blood supply to a larger or smaller area of ​​the limb, up to its gangrene;
• if the plaque blocks the aorta in the area where large vessels originate from it to each of lower limbs, both legs will suffer only from ischemia or gangrene.

How to determine if there are cholesterol plaques

Before cleaning blood vessels from cholesterol plaques and blood clots, you need to find out whether they are there or not. If the lipid profile shows the risk of plaque formation, the coagulogram shows the risk of thrombus formation, then instrumental studies will help to detect immediate “congestion” in the vessels:

• A special type of ultrasound is color duplex scanning . In this way it is very convenient to examine the arterial and venous vessels of the upper and lower extremities, the aorta, the vessels going to the brain and those that nourish the retina;
• Triplex scanning is another ultrasound option. It is used to examine the vessels of the brain and the arteries that supply it - those located outside the cranial cavity;
• Most exact method research – angiography. It is used to clarify the location of plaques/thrombi in the vessels of the extremities that were identified during duplex or triplex scanning, as well as to determine blood clots/plaques in those organs that cannot be seen during ultrasound examination.

When to clean vessels

You need to clear cholesterol from your blood vessels when:

• according to instrumental methods atherosclerotic plaques or
• when there is already a violation internal organs, against which a high atherogenic index was detected (according to lipid profile). This:
  • cholesterol above 6.19 mmol/l;
  • LDL – more than 4.12 mmol/l;
  • HDL: below 1.04 for men, below 1.29 mmol/l for women.

In the following cases, it is necessary to do everything possible to prevent the deposition of cholesterol on the walls of blood vessels:

• men over 40 years old;
• women over 55 years old;
• if you have bad habits;
• if a person eats a lot of smoked, fried, salty food, meat;
• if relatives have atherosclerosis, ischemic or hypertension;
• those suffering diabetes mellitus;
• those who note the presence of excess weight;
• those who have suffered a complication of streptococcal infections such as rheumatism;
• if at least once there was numbness of one limb or half of the body, which did not follow their compression, but arose “by itself”;
• if at least once there was a visual impairment in one eye, which then went away;
• when there was an attack of sudden general weakness;
• if there is causeless pain in the navel area, accompanied by flatulence and constipation;
• when memory deteriorates, and the desire to rest causes less and less mental stress;
• if it becomes more and more difficult to walk, your legs hurt with less and less load;
• when there is chest or heart pain that is not relieved by nitroglycerin;
• if the hair on your legs falls out, and your legs themselves turn pale and freeze;
• if any ulcers, redness, or swelling begin to appear on the lower extremities.

What you need to do before you start cleaning blood vessels from plaques

In order not to encounter the fact that cleaning blood vessels at home will result in blood clots or plaques being pulled away from the walls with corresponding consequences, before carrying out it you need to be examined:

1. take a coagulogram so that the laboratory can determine not only standard indicators, but also the INR index;
2. take a lipid profile;
3. Be sure to perform an electrocardiogram.

How to cleanse blood vessels from atherosclerotic plaques

The program for cleaning blood vessels from cholesterol deposits on their walls should be left by the doctor based on the results of laboratory and instrumental studies. It must include:

1. lifestyle changes if they lead to the formation of plaques;
2. adherence to a diet that will lead to the normalization of the functioning of the digestive organs, so that “good” cholesterol is best absorbed;
3. a diet that will prevent blood clots.

According to indications, the following may be prescribed:

1. medications that reduce blood cholesterol levels;
2. drugs that reduce blood viscosity;
3. folk remedies aimed at normalizing blood viscosity or reducing cholesterol levels.

Step 1. Do not let “bad” cholesterol increase

Without this action, all further measures - whether folk recipes, drugs - will not have the desired effect, since the person will continue to saturate the body with cholesterol.

This can only be done with diet:

• when dishes are prepared by baking or boiling;
• there is a sufficient amount of porridge;
• with lots of vegetables and fruits;
• with products containing polyunsaturated omega-3 fatty acids;
• when there is enough seafood;
• dairy products are low-fat.

You need to exclude:

Step 2. Diet to stop blood clots

To prevent the formation of blood clots on atherosclerotic plaques, which are dangerous because they can break off at any time, follow the following diet (it is almost identical to the one that limits the intake of cholesterol:

Step 3. Lifestyle changes

Without such measures, the following steps are ineffective. Otherwise, blood will stagnate in the vessels, which is very popular with blood clots and atherosclerotic plaques. As measures to “clean” blood vessels, you need to:

• sleep enough time, as dictated by the endocrine and nervous systems. When the organs that make them up come into balance, they will also try to ensure a normal balance between the coagulation and anticoagulation, atherosclerotic and anti-atherosclerotic systems;
• move more, eliminating blood stagnation;
• visit more often fresh air, providing a sufficient flow of oxygen;
• prevent the formation of excess weight;
• control blood glucose levels, whose increased level damages blood vessels;
• prevent long-term existence arterial hypertension, which also deforms the vascular wall;
• follow the principles of the diet described above.

Step 4. Drugs to cleanse blood vessels from blood clots

To prevent blood clots, tablets are used to prevent the deposition of platelets on the walls of blood vessels. These are “Thrombo-Ass”, “CardioMagnil”, “Plavix”, “Clopidogrel”, “Aspecard”, “Curantil” and others.

If the INR is low according to the coagulogram, anticoagulant drugs are prescribed and there are atherosclerotic plaques or blood clots; not only the aspirin-based antiplatelet agents mentioned above are prescribed, but also drugs that affect the blood coagulation system. This injectable drugs"Clexan", "Fragmin", "Fraxiparin", in the worst case - injectable "Heparin". You can also use the drug "Warfarin". The dosage is selected by the doctor. After starting to take such drugs, be sure to monitor the INR by adjusting the dose of the drug, otherwise bleeding may begin.

Step 5. Hirudotherapy

Treatment with medicinal leech bites prevents the formation of blood clots in blood vessels. This occurs due to the fact that this worm, when sucking, releases various enzymes into the blood. They should serve to ensure that while the leech drinks blood, it does not clot. As a result, hirudin and other enzymes enter the systemic bloodstream, dissolving existing small blood clots and preventing further thrombus formation.

Hirudotherapy cannot be performed by everyone, but only in the absence of:

• blood clotting disorders;
• exhaustion;
• pregnancy;
• caesarean section or other surgery performed within 4 months ago;
• hypersensitivity to one of the components of leech “saliva”;
• persistent low blood pressure.

Before you cleanse blood vessels with folk remedies, consult your cardiologist or therapist to see if you can take this or that decoction.

• rowan;
• white willow bark;
• tansy;
• nettle;
• strawberry leaves;

For the same purpose, you can purchase certified dietary supplements in herbal pharmacies: hawthorn and rosehip syrup, “Beets with celery,” “Hawthorn Premium.” If you don’t like the taste of garlic, buy the dietary supplement “Garlic Powder” from Solgar. Ginkgo biloba, produced in the form of dietary supplements, thins the blood very well.

Common folk recipes

Here are the 2 most common recipes.

• You need garlic and lemon. You need to take them by weight in equal quantities and grind them in a meat grinder. Now add the same amount of honey as this mixture, stir. Leave for a week in a sealed container, stirring occasionally. Drink the mixture once a day, 4 teaspoons.
• Take 5 tbsp. pine needles, 3 tbsp. rose hips, 1 tbsp. onion peel. Pour this mixture into 1 liter cold water, then bring the infusion to a boil and simmer for 10 minutes. Then turn off the heat, cover the pan and leave overnight. In the morning, strain the mixture and drink it in small portions throughout the day.

A possible step is drugs to dissolve cholesterol plaques

In some cases, with a high atherogenic index (determined by a blood test for lipids), it is advisable to prescribe drugs that will dissolve atherosclerotic plaques. Only a cardiologist or therapist makes such a prescription, since only he is able to assess the balance between the risk of side effects and the potential benefits of these drugs.

There are 2 main types of cholesterol-lowering drugs prescribed. These are statins (Atorvacard, Simvastatin, Lovastatin and others) and fibrates (Clofibrate, Tycolor, Esklip).

Statins

Statins are drugs that lower cholesterol by blocking the enzyme pathway by which it is synthesized. Although these medications are included in the plan compulsory treatment atherosclerosis, prescribed by the Ministry of Health, but due to the large number of side effects, the doctor will think whether it is worth prescribing them, or whether treatment can be carried out without their use. They are mandatory for use by the following categories of persons:

• during acute period myocardial infarction;
• those who have had a heart attack or stroke;
• before and after heart surgery;
• severe coronary heart disease, when the level of myocardial infarction is high.

With a low risk of developing a heart attack, in the presence of diabetes mellitus, as well as in women before menopause, the use of such drugs can cause side effects from any of the body systems. If you try to treat only high cholesterol levels with statins, when a person’s heart, kidneys and liver are healthy, it is quite risky, especially since the harmful effects here develop gradually, gradually. But if you have already decided to cleanse the vessels in this way, you need to monitor your blood biochemical parameters monthly, especially what is called “liver tests.” It is also not worth reducing or increasing the dosage on your own.

Fibrates

These are drugs that reduce the production of cholesterol: Clofibrate, Gemfibrozil, Tycolor and others. They are not as good at lowering cholesterol as statins, but they are not as toxic either. These 2 groups of drugs are most often combined to reduce the number of side effects.

Other groups of drugs

In some cases, drugs that are aimed at reducing cholesterol intake are effective. These are Orlistat, Xenical, Ezetrol. Their effectiveness is not as high as that of statins or fibrates, since most of the “bad” lipoproteins are still produced by the body and are not absorbed from food.

In the absence of indications for taking statins, but in the presence of diabetes mellitus, hypertension, chronic cholecystitis or cholelithiasis, such a bad habit as smoking, dietary supplements can be used. Such products, which are available in capsules or tablets and are not considered “real” drugs, are sometimes no less effective in clearing plaque from blood vessels without causing huge amount unpleasant side symptoms. These are “Tykveol”, “Lipoic acid”, “Omega Forte”, “Doppelgerts omega 3”, “CardioActive Hawthorn”, “Golden mumiyo”.

Possible step - surgery

When an atherosclerotic plaque is “overgrown” with calcium salts so that no drug reaches its cholesterol core or folk remedy. At the same time, it does not provide nutrition to any organ or threatens the development of a stroke or gangrene. In this case, the only solution is surgery to remove plaque from the vessels. At the same time, a “bypass” is created for the blood supply to the suffering organ, for example, coronary artery bypass surgery, when an additional “path” is created from the overlying area to the vessel that goes directly to the tissue in need. Thus, the blood flows past the “clogged” area of ​​the vessel. Sometimes a stenting operation is performed, when a “tube” (stent) is placed in the area of ​​the narrowed artery, returning the vessel to its original lumen diameter.

After such interventions, long-term use of drugs that reduce blood clots together with drugs that will maintain normal cholesterol levels is necessary to prevent the re-formation of plaques.

Thus, if you want to protect your blood vessels from possible plaque deposits, you need to adjust your lifestyle, take a course of decoctions or infusions prepared according to folk recipe. The same applies to people who do not complain of heart problems and discover that they have high cholesterol levels in their blood. If, while walking, performing physical activity, or when getting out of bed, behind the sternum or on the left side chest pain or discomfort appears, if you suffer from high blood pressure or have previously been diagnosed with a heart defect, you should consult your doctor about the advisability of taking cholesterol-lowering drugs.

Remember: don’t get too carried away with lowering cholesterol. This element is needed for the membranes of each of our cells; a small amount of it increases the risk of developing cancer, diseases of the nervous system, including stroke, as well as a condition in which there is a low content of hemoglobin in the blood - anemia.

Proteins involved in the development of Alzheimer's disease are present in the brain of every person, but despite this, the vast majority of people do not get sick and will never get sick. Alzheimer's disease. What lies at the heart of this “inequality”?

β-secretase(BACE) is involved in the breakdown
amyloid precursor protein(ARR)
with education beta amyloid(β-amyloid),
which aggregates, forming characteristic
Alzheimer's disease extracellular
senile plaques (β-amyloid plaque).
(Fig. withfriendship.com)

Why don't we all get Alzheimer's disease? For the cell biologist Subojita Roy Subhojit Roy, MD, PhD, this question is of particular interest because Dr. Roy is an associate professor in the departments of pathology and neurology at the University of California, San Diego School of Medicine.

In an article published in the magazine Neuron, Dr. Roy and his colleagues explain this phenomenon: in their opinion, the wisdom of nature is that most people maintain the vital physical separation of protein and its enzyme, the interaction of which is the trigger for the progressive degeneration and cell death characteristic of the disease Alzheimer's.

“This can be compared to the physical separation of gunpowder and matches, preventing an inevitable explosion,” says Dr. Roy. “By knowing exactly how these gunpowder and matches are separated, we can develop new insights into how to stop the disease.”

The severity of Alzheimer's disease is assessed by the loss of functional neurons. There are two “tell-tale” signs of this disease: protein clots beta amyloid- so called beta amyloid plaques, - accumulating outside neurons, and aggregates of another protein called tau, forming neurofibrillary tangles inside nerve cells. Most neuroscientists believe that Alzheimer's disease is caused by the formation and accumulation of beta-amyloid plaques, which trigger a cascade of molecular events leading to cell dysfunction and death. So this so-called "amyloid cascade hypothesis" places beta-amyloid at the center of the pathology of Alzheimer's disease.

Beta-amyloid requires interaction to form amyloid precursor protein(APP) and enzyme beta-secretase(BACE), which breaks down APP into smaller toxic fragments.

Top: bubbles containing APP(green)
And BACE(red) usually physically
separated. Bottom: after neuron stimulation,
increasing synthesis beta amyloid, bubbles
with APP and BACE converge (shown in yellow),
and the proteins begin to interact.
(Photo: UC San Diego School of Medicine)

“Both of these proteins are expressed in the brain at high level“, explains Dr. Roy, “and if you let them interact continuously, we will all get Alzheimer's disease.”

However, this does not happen. By experimenting with cultured hippocampal neurons and human and mouse brain tissue, Dr. Roy and his colleagues found that in healthy brain cells, BACE-1 and APP tend to be separated and reside in different compartments from the moment they are formed, which excludes their contact.

“To separate these accomplices, nature seems to have come up with an interesting trick,” comments Dr. Roy.

In addition, it turned out that conditions that enhance the synthesis of beta-amyloid protein also enhance the interaction between APP and BACE-1. In particular, increasing electrical activity neurons - which, as is known, stimulates the synthesis of beta-amyloid - also leads to increased interaction between APP and BACE-1. A study of autopsy brain samples from patients with Alzheimer's disease showed an increase in the physical proximity of these proteins, confirming the pathophysiological significance of this phenomenon.

The study's findings are critical because they illuminate some of the earliest molecular trigger events for Alzheimer's disease and show how healthy brains are protected from them. From a clinical point of view, they outline new possible directions in the treatment or even prevention of the disease.

To a certain extent, this is an unconventional approach. But, according to the first author of the article, Dr. Utpala Dasa(Utpal Das), “The exciting thing is that we may be able to screen for molecules that can physically separate APP and BACE-1.”

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Older age and the buildup of amyloid beta protein plaques in brain tissue contribute to the development of a devastating form of dementia known as Alzheimer's disease. The results of the study provided evidence for scientists The fact that vitamin D affects the process of transporting proteins, which helps naturally clear the brain of their accumulation.

Vitamin D can dramatically change the development and progression of many diseases, including cancer, heart disease and diabetes. vegan recipes on likelida.com Today, scientists believe that Alzheimer’s disease can also be included in this list. Getting vitamin D by staying under sun rays or when taking prohormone supplements should be considered mandatory for all people wishing to.

Vitamin D helps clear the brain of deadly amyloid protein plaques

During the experiment, scientists used data on the health of laboratory mice genetically predisposed to developing dementia. At the same time, the animals were given injections of vitamin D. It was found that this vitamin selectively prevents the accumulation of beta-amyloid, and special transport proteins clear cells of destructive amyloids before they can accumulate. The brain has a number of special transport proteins known as LRP-1 and P-GP that escort amyloid proteins across the blood-brain barrier before they can cause any harm.

Researchers believe that vitamin D improves the movement of beta-amyloid across the blood-brain barrier by regulating protein expression through receptors. At the same time, vitamin D also regulates the transmission of cell impulses through the MEK metabolic pathway. The results of these experiments showed scientists new ways to solve problems related to the treatment and prevention of Alzheimer's disease.

Controlling vitamin D levels in the blood reduces the risk of developing Alzheimer's dementia

Researchers believe that vitamin D helps transport beta-amyloid protein structures across the sensitive blood-brain barrier, helping to separate clusters in the cerebrospinal fluid for subsequent elimination. This ability is known to decline with age, allowing sticky protein clusters to accumulate around neuronal synapses. Scientists have found that older adults diagnosed with Alzheimer's disease tend to have low level vitamin D. B this moment Researchers have established a connection between the level of blood saturation with this vitamin and the development of diseases.

The study authors do not say what the optimal level of vitamin D should be. However, the results of many previous experiments have shown that the best blood level of this substance to be possible is 50-80 ng/ml. Most health-conscious people need to take an oil-based vitamin D supplement to fully protect themselves from this fatal form of dementia.

Documents of universities, institutes, universities, academies. Buy a diploma in Moscow on the website diplomzakaz.com

Scientists at the University of Michigan have discovered a new useful property epigallocatechin gallate (EGCG) is a bioactive substance contained in green tea leaves. The results of their study show that EGCG prevents the misfolding of certain brain proteins, including those associated with development. Alzheimer's disease. (Photo: University of Michigan)

Scientists at the University of Michigan ( University of Michigan, U-M) have discovered a new beneficial property of one of the molecules contained in green tea: it prevents the misfolding of specific brain proteins. The aggregation of these proteins, called metal-associated beta-amyloids, associated with Alzheimer's disease and others neurodegenerative diseases .

U-M Life Sciences Institute Associate Professor Mi Hee Lim, PhD, and an interdisciplinary team of scientists studied the effect of green tea extract on aggregate formation metal-associated amyloid beta in vitro. The results of their experiments are presented in a paper recently published in the journal Proceedings of the National Academy of Sciences .

Scientists have found that in vitro a compound found in green tea epigallocatechin-3-gallate(epigallocatechin-3-gallate, EGCG) interacts more actively with metal-associated beta-amyloids (containing, in particular, copper, iron and zinc) than with metal-free peptides, forming small unstructured aggregates. In addition, when live cells were incubated with EGCG, the toxicity of both metal-free and metal-bound amyloid beta was reduced.

Associate Professor, Department of Chemistry, Life Sciences Institute, U-M Mi Hee Lim, PhD. (Photo: lsi.umich.edu)

To gain insight into the structure of interactions and understand this reactivity at the molecular level, the scientists used ion mobility mass spectrometry (IM-MS), 2D NMR spectroscopy and computational methods. Experiments have shown that EGCG interacts with amyloid beta monomers and dimers to form more compact peptide conformations than when bound to untreated EGCG amyloid beta. In addition, ternary EGCG–metal–Aβ complexes were formed.

Dr. Lim's research team consisted of chemists, biochemists and biophysicists.

“There is a lot of interest in this molecule from a lot of scientists,” says Dr. Lim, noting that EGCG and other flavonoids found in natural foods have long been recognized as powerful antioxidants. "We used A complex approach. This is the first example of an interdisciplinary study that focused on structure, conducted by three scientists from three different fields of science.”

According to Lim, although small molecules metal-associated amyloid beta are studied by many scientists, most of the researchers consider them from their own, narrow point of view.

Neuroscientist Bing Ye. (Photo: umms.med.umich.edu)

"But because the brain is so complex, we think a combination of approaches is needed."

Article in PNAS is the starting point, the scientist continues, and next step The study will test the ability of a slightly modified EGCG molecule to inhibit plaque formation in fruit flies.

“We want to modify the molecule so that it specifically interferes with the formation of plaques associated with Alzheimer's disease,” explains Lim.

She plans to continue her work in collaboration with LSI neuroscientist Bing Ye. Together, the researchers will test the new molecule's ability to inhibit the potential toxicity of aggregates containing proteins and metals in fruit flies.

Based on materials

Original article:

S.-J. Hyung, A. S. DeToma, J. R. Brender, S. Lee, S. Vivekanandan, A. Kochi, J.-S. Choi, A. Ramamoorthy, B. T. Ruotolo, M. H. Lim. Insights into antiamyloidogenic properties of the green tea extract (-)-epigallocatechin-3-gallate toward metal-associated amyloid-β species

© "Green tea extract prevents the formation of beta-amyloid plaques in Alzheimer's disease." Full or partial reprinting of the material is permitted provided that the active hyperlink to the page is not blocked from indexing and is not prohibited for the robot to follow Alzheimer's disease. Written permission is required.

More about Alzheimer's disease

– a general, systemic disease of the body in which a specific glycoprotein (amyloid) is deposited in organs and tissues with impaired function of the latter. Amyloidosis can affect the kidneys ( nephrotic syndrome, edema syndrome), heart (heart failure, arrhythmias), gastrointestinal tract, musculoskeletal system, skin. Possible development of polyserositis, hemorrhagic syndrome, mental disorders. Reliable diagnosis of amyloidosis is facilitated by the detection of amyloid in biopsy samples of affected tissues. To treat amyloidosis, immunosuppressive and symptomatic therapy is carried out; according to indications - peritoneal dialysis, kidney and liver transplantation.

ICD-10

E85

General information

Amyloidosis is a disease from the group of systemic dysproteinoses that occurs with the formation and accumulation in tissues of a complex protein-polysaccharide compound - amyloid. The prevalence of amyloidosis in the world is largely geographically determined: for example, periodic disease is more common in the countries of the Mediterranean basin; amyloid polyneuropathy - in Japan, Italy, Sweden, Portugal, etc. Average frequency amyloidosis in the population is 1 case per 50 thousand population. The disease usually develops in people over 50-60 years of age. Considering the fact that amyloidosis affects almost all organ systems, the disease is studied by various medical disciplines: rheumatology, urology, cardiology, gastroenterology, neurology, etc.

Causes of amyloidosis

The etiology of primary amyloidosis has not been fully studied. However, it is known that secondary amyloidosis is usually associated with chronic infectious (tuberculosis, syphilis, actinomycosis) and purulent-inflammatory diseases (osteomyelitis, bronchiectasis, bacterial endocarditis, etc.), less often - tumor processes(lymphogranulomatosis, leukemia, cancer visceral organs). Reactive amyloidosis can develop in patients with atherosclerosis, psoriasis, rheumatoid pathology (rheumatoid arthritis, ankylosing spondylitis), chronic inflammation (ulcerative colitis, Crohn's disease), multisystem lesions (Whipple's disease, sarcoidosis). Among the factors contributing to the development of amyloidosis, hyperglobulinemia and dysfunction cellular immunity, genetic predisposition, etc.

Pathogenesis

Among the numerous versions of amyloidogenesis, the theory of dysproteinosis, local cellular genesis, immunological and mutation theories has the largest number of supporters. The theory of local cellular genesis considers only processes occurring at the cellular level (the formation of fibrillar amyloid precursors by the macrophage system), while the formation and accumulation of amyloid occurs outside the cell. Therefore, the theory of local cell genesis cannot be considered exhaustive.

According to the theory of disproteinosis, amyloid is a product of abnormal protein metabolism. The main links in the pathogenesis of amyloidosis - dysproteinemia and hyperfibrinogenemia - contribute to the accumulation of coarse fractions of protein and paraproteins in the plasma. The immunological theory of the origin of amyloidosis associates the formation of amyloid with the antigen-antibody reaction, in which the antigens are foreign proteins or breakdown products of one's own tissues. In this case, amyloid deposition occurs predominantly in areas of antibody formation and excess antigens. The most universal is mutation theory amyloidosis, taking into account a huge variety of mutagenic factors that can cause abnormal protein synthesis.

Amyloid is a complex glycoprotein consisting of fibrillar and globular proteins closely associated with polysaccharides. Amyloid deposits accumulate in the intima and adventitia blood vessels, stroma of parenchymal organs, glandular structures, etc. With minor amyloid deposits, changes are detected only at the microscopic level and do not lead to functional disorders. Severe amyloid accumulation is accompanied by macroscopic changes in the affected organ (increased volume, greasy or waxy appearance). As a result of amyloidosis, stromal sclerosis and atrophy of the organ parenchyma and their clinically significant functional failure develop.

Classification

According to the causes, there are primary (idiopathic), secondary (reactive, acquired), hereditary (familial, genetic) and senile amyloidosis. There are various forms of hereditary amyloidosis: Mediterranean fever, or periodic illness (fever attacks, abdominal pain, constipation, diarrhea, pleurisy, arthritis, skin rashes), Portuguese neuropathic amyloidosis (peripheral polyneuropathy, impotence, cardiac conduction disorders), Finnish type ( corneal atrophy, cranial neuropathy), Danish variant (cardiopathic amyloidosis) and many others. etc.

Depending on the predominant damage to organs and systems, nephropathic (amyloidosis of the kidneys), cardiopathic (amyloidosis of the heart), neuropathic (amyloidosis of the nervous system), hepapathic (amyloidosis of the liver), epinephropathic (amyloidosis of the adrenal glands), ARUD amyloidosis, skin amyloidosis and a mixed type of disease are distinguished. . In addition, in international practice it is customary to distinguish between local and generalized (systemic) amyloidosis. To localized forms, usually developing in individuals old age, include amyloidosis in Alzheimer's disease, type 2 diabetes mellitus, endocrine tumors, skin tumors, Bladder etc. Depending on the biochemical composition of amyloid fibrils, the following types are distinguished among systemic forms of amyloidosis:

• AL- in the composition of fibrils Ig light chains (for Waldenström's disease, multiple myeloma, malignant lymphomas);
• A.A.– the fibrils contain acute-phase serum α-globulin, similar in its characteristics to C-reactive protein (for tumor and rheumatic diseases, periodic illness, etc.);
• Aβ2M- contains β2-microglobulin fibrils (for chronic renal failure in patients on hemodialysis);
• ATTR– the fibrils contain the transport protein transthyretin (in familial hereditary and senile forms of amyloidosis).

Symptoms of amyloidosis

Clinical manifestations of amyloidosis are diverse and depend on the severity and localization of amyloid deposits, the biochemical composition of amyloid, the duration of the disease, and the degree of organ dysfunction. In the latent stage of amyloidosis, when amyloid deposits can only be detected microscopically, there are no symptoms. As the functional insufficiency of a particular organ develops and progresses, the clinical signs of the disease increase.

With renal amyloidosis, the long-term stage of moderate proteinuria is replaced by the development of nephrotic syndrome. The transition to the advanced stage may be associated with an intercurrent infection, vaccination, hypothermia, or exacerbation of the underlying disease. Swelling gradually increases (first in the legs and then throughout the body), nephrogenic arterial hypertension and renal failure develop. Renal vein thrombosis may occur. Massive protein loss is accompanied by hypoproteinemia, hyperfibrinogenemia, hyperlipidemia, and azotemia. Micro-, sometimes macro-hematuria and leukocyturia are detected in the urine. In general, during renal amyloidosis, an early non-edematous stage, an edematous stage, and a uremic (cachectic) stage are distinguished.

Cardiac amyloidosis occurs as a restrictive cardiomyopathy with typical clinical signs– cardiomegaly, arrhythmia, progressive heart failure. Patients complain of shortness of breath, swelling, and weakness that occurs with minor physical exertion. Less commonly, with cardiac amyloidosis, polyserositis develops (ascites, exudative pleurisy and pericarditis).

Damage to the gastrointestinal tract in amyloidosis is characterized by amyloid infiltration of the tongue (macroglassia), esophagus (rigidity and impaired peristalsis), stomach (heartburn, nausea), intestines (constipation, diarrhea, malabsorption syndrome, intestinal obstruction). Gastrointestinal bleeding may occur at various levels. With amyloid infiltration of the liver, hepatomegaly, cholestasis, and portal hypertension develop. Damage to the pancreas due to amyloidosis is usually disguised as chronic pancreatitis.

Amyloidosis of the skin occurs with the appearance of multiple waxy plaques (papules, nodules) in the face, neck, and natural skin folds. By external signs the skin lesions may resemble scleroderma, neurodermatitis, or lichen planus. For amyloid lesions of the musculoskeletal system, the development of symmetrical polyarthritis, carpal tunnel syndrome, glenohumeral periarthritis, and myopathy is typical. Individual forms amyloidosis involving the nervous system may be accompanied by polyneuropathy, paralysis of the lower limbs, headaches, dizziness, orthostatic hypotension, sweating, dementia, etc.

Diagnostics

), endoscopic studies(EGD, sigmoidoscopy). Amyloidosis should be thought of when proteinuria, leukocyturia, cylindruria are combined with hypoproteinemia, hyperlipidemia (increased blood levels of cholesterol, lipoproteins, triglycerides), hyponatremia and hypocalcemia, anemia, and a decrease in platelet count. Electrophoresis of blood serum and urine allows you to determine the presence of paraproteins.

A definitive diagnosis of amyloidosis is possible after detection of amyloid fibrils in the affected tissues. For this purpose, a biopsy of the kidney, lymph nodes, gums, gastric mucosa, and rectum can be performed. Establishing the hereditary nature of amyloidosis is facilitated by a thorough medical-genetic analysis of the pedigree.

Treatment of amyloidosis

The lack of complete knowledge about the etiology and pathogenesis of the disease causes difficulties associated with the treatment of amyloidosis. In case of secondary amyloidosis, active treatment of the underlying disease is important. Dietary recommendations suggest limiting the intake of table salt and protein, and including raw liver in the diet. Symptomatic therapy for amyloidosis depends on the presence and severity of certain clinical manifestations. As pathogenetic therapy, drugs of the 4-aminoquinoline series (chloroquine), dimethyl sulfoxide, unithiol, colchicine can be prescribed. For the treatment of primary amyloidosis, treatment regimens with cytostatics and hormones (melfolan + prednisolone, vincristine + doxorubicin + dexamethasone) are used. With the development of chronic renal failure, hemodialysis or peritoneal dialysis is indicated. In some cases, the question of kidney or liver transplantation is raised.

Forecast

The course of amyloidosis is progressive, almost irreversible. The disease may be aggravated by amyloid ulcers of the esophagus and stomach, bleeding, liver failure, diabetes mellitus, etc. With the development of chronic renal failure average duration the life of patients is about 1 year; with the development of heart failure - about 4 months. The prognosis of secondary amyloidosis is determined by the possibility of treating the underlying disease. A more severe course of amyloidosis is observed in older patients.