Biochemical alterations.

Schizophrenia could be the consequence of a communication problem between neurons. Of all the neurotransmitters (those responsible for transmitting information between neurons), it has been seen that dopamine (a neurotransmitter present in various areas of the brain and which is especially important for the body’s motor function) is the one that is most altered. Classically, the hypothesis that there is an imbalance of dopaminergic function has been the main neurochemical hypothesis of schizophrenia, postulating that the disease, or at least the psychotic symptoms, are the result of an excess of dopaminergic activity. The main strength of this hypothesis is based on the fact that drugs that reduce dopamine improve psychosis, while drugs that increase it can trigger symptoms of this type or aggravate schizophrenia.

Alterations in the structure of the brain.

About half of the patients present alterations in the structure of the brain. These include dilation of the ventricles, a decrease in the volume of certain areas of the brain (especially the temporal lobe, the tonsil-hippocampal formation, the thalamus, the prefrontal cortex) and an overall decrease in the size of the brain. However, it is important to note that these alterations are not specific to schizophrenia, nor do all patients present them.

Alterations in the functioning of the brain.

Most of the functional neuroimaging studies, in which not only the structure of the brain is studied but also the function, have indicated a decrease in the function of the prefrontal cortex in schizophrenia, which is the part of the brain that gives the ability to reasoning. This hypofrontality constitutes one of the most widely contrasted biological findings of schizophrenia. Hypofrontality is more evident during mental tests that require prefrontal activation.

Despite all the research and the great advances that have been made in the last forty years, there are no complementary diagnostic tests that ensure the diagnosis of the disorder.

The onset of symptoms of the disease, typically in late adolescence, occurs when the structures involved reach their functional maturity, since the maturation of the brain does not end in adolescence but continues into adulthood in which some are eliminated. useless neurons and circuits through complex processes, such as preprogrammed neuronal and synaptic cell death (apoptosis). At present it is also known that certain inflammatory and immunological phenomena could be involved in the appearance and progression of schizophrenia.

Risk factor’s

A risk factor is a condition that does not cause a certain disease, but is associated with it. For example, high cholesterol (hypercholesterolemia) acts as a risk factor for heart attack. It does not mean that it causes it, because not all people with high cholesterol will have a heart attack, and not all people with a heart attack have high cholesterol. But it does mean that the chances of having a heart attack are increased.

Thus, various risk factors have been found that increase the chances of having schizophrenia, although not directly causing it.

The genetic factor is the most important and it is estimated that it accounts for 80% of the disease. The probability of a case of schizophrenia occurring in a family is higher if another family member is already diagnosed with the disease.

Depending on the degree of kinship with the affected family member, the risk increases or decreases. Does this mean that schizophrenia is a genetic disease? If by genetic disease you mean a disease caused by a single gene, the answer is no. The weight of genetics in this disease is enormous (around 80%), but not in a single gene.

The most current theories indicate that the presence of a number of altered genes predisposes to have the disease. That is, like other complex medical conditions, such as diabetes, it takes more than one altered gene to develop the disease. This inheritance predisposes to a greater vulnerability to develop schizophrenia in the face of certain environmental factors that would trigger the appearance of the clinical picture.

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