Did you know that when the brain is affected by Alzheimer's disease, irreversible processes occur, so today this disease is considered incurable? There are several reasons for disruption of cells, which will be discussed below.

It is important to note that even though medical research is conducted, Alzheimer's disease is still a mystery to doctors.

Post information is based on data from the course «Understanding Alzheimer's Disease: Molecular and Genetic Approaches».

Let me start with the history.

HISTORY OF DISEASE DISCOVERING

The history of the discovery of Alzheimer's disease started with two names: Alois Alzheimer and Auguste Deter, the first of whom was a psychiatrist, and the second one — a patient who was diagnosed for the first time with an unknown disease.

Auguste Deter was about 40 years old when she began to suffer from dementia, paranoia, memory loss, hallucinations and autonomic disorders. Dr. Alzheimer, after examining her brain, noticed some pathologies — then such changes did not have a special name and only thanks to Kraepelin Emil who also studied biological bases of diseases and was the mentor of Alois, he introduced the concept of «Alzheimer's disease» in 1910. At that time the discovery did not become popular in medical field; a renewed interest in Alzheimer's research was demonstrated by Bernard Tomlinson and two more doctors in 1968. A detailed review of biochemical analyzes of patients confirmed the idea of Alzheimer, offered more than half a century ago.

RESEARCH PIONEERS OF THE BRAIN DISEASE

To date, more than 30,000 studies have been performed on senile disease. All of them are based on data from researchers working in a particular industry and looking for the root causing the disease. There were six doctors who made an individual incredible contribution to medicine and studied Alzheimer's disease in particular.

1. Theodor Schwann. German physiologist, cytologist, histologist, who developed the cellular theory of the disease development.
2. Rudolf Virchow. German physiologist, who determined pathological basis of the disease, «withdrew» medicine from the humoral theory.
3. Santiago Ramon y Cajal. Spanish doctor, innovator in neuroscience.
4. Gheorghe Marinescu. Romanian scientist who described senile plaques.
5. Paul Oscar Blocq. French pathologist who also dealt with the issue of senile plaques.
6. Emil Redlich. Austrian neurologist and psychiatrist discovered senile plaques and introduced this term into medical vocabulary.

MORPHOLOGY OF SENILE PLAQUES APPEARANCE

In Alzheimer's disease, senile (amyloid) plaques accumulate in the brain6 tese are deposits of beta amyloid protein of round shape. These formations have a spherical shape about 0.2 mm in size and are insoluble. As a rule, senile plaques are surrounded by altered neurons that have pathology and contain neurofibrillar plexuses. During interaction, a neuronal cell dies and a neurofibrillary plexus is released into the space between the cells.

Screenshot of the course

The thuth is that senile plaques are formed in all older people, but only their abundant number indicates a pathology. The main component of senile plaques is beta-amyloid, which is formed from the precursor of beta-amyloid (PBA). Its main species are a peptide of 40 amino acid residues and a peptide of 42 amino acid residues. To convert proteins into one another, special secretase substances are needed (alpha-secretase splits beta amyloid straight in the center, beta-secretase cuts the chain of beta amyloid precursor from the inside, gamma-secretase cuts the PBA chain in the transmembrane zone, which creates peptides of different length). So deposits appear in the brain tissues, and they constitute the morphological feature of the disease. In this case, beta-amyloid is a common protein synthesized by the body, so the theory suggests that a more detailed study of the biochemistry of this protein and its precursor can give a clue to Alzheimer's disease.

Among causes of disease appearance there is heredity, but the percentage of cases when the disease is activated is very low, only 1%. If a person has inherited a certain gene, this does not mean that the disease will definitely acquire development, because in addition to heredity, other factors play an important role.

The hereditary gene includes three types: a precursor of beta-amyloid, presenelin-1 and presenilin-2.

Scientists distinguish another gene, which is at risk, — apolipoprotein. About a quarter of the people on earth are its carriers and possible further pathology is very dependent on unfavorable external environment. Plus, new research shows that, in addition, there is a large number of other genes that increase the risk of the disease.

IS HEALTHY LIFESTYLE PREVENTIVE?

There is no scientific 100-percent «yes» to this question yet. Undoubtedly, a balanced diet, exercise, calm inner state positively affect the body on the whole, but to make these guesses become scientific statistics, more research is needed.

The data that is available todayinforms that a healthy lifestyle can reduce the risk by at least 50%.

People live in a very polluted environment, so according to the toxic theory in the body, nitrates accumulate throughout life, which in old age destroy brain neurons.

But the research of Dr. Perry, who previously studied fish and animals in the context of the environment, gives the idea that humans are adaptive creatures and that the occurrence of amyloids is nothing more than a normal reaction to aging. Dr. Perry argues that pathology does not necessarily have negative effects, it is rather a response and adaptation of the organism to conditions. After all, a group of patients with Alzheimer's disease recovered amyloids, but their condition did not improve. This makes us think that the reason is different. Maybe people in whose brain senile plaques were found should not be considered pre-patients, but it might be assumed that their brains have created plaques to maintain themselves in the norm. The doctor does not deny any of the studies conducted by other scientists, but shows a non-working hypothesis that simple removal of amyloid plaques does not improve the patient's condition.

In the next post I will tell you what a tau protein is and about its connection with senile plaques.

Photos are under license CC0, if not specified.