The man's brain ages before the woman's brain:

Men's brains age worse than women's. The speed at which the brain atrophies is greater in males than in women and age worse, especially from the age of 80 years. This is one of the conclusions of the study carried out by researchers from the Universitat Politècnica de València (UPV), the Universitat de València (UV) and the National Centre for Scientific Research of France-CNRS, in its French acronym, and published in the Human Brain Mapping magazine.

The work offers answers to the questions how the brain changes throughout our lives, what are the normal values of the volumes of the brain structures or if there are differences in the development of the brain throughout the life between men and Women.
A team of computer scientists, neurologists and biologists from these three centers have developed one of the most exhaustive studies carried out to date on the development of the human brain, by number of cases analyzed and age range evaluated, since it covers from That we are babies until old age, the academic institutions stand out through a statement.
In total, they have analyzed 2,944 images of brain magnetic resonance, healthy subjects aged between nine months and 95 years. Of all of them, 1,379 were women and 1,565 men. The images belong to public databases of nine European, American and Australian institutions.
In their study, they analyzed the volumes of the hippocampus, amygdala, putamen, accumbens, Globus palidus, thalamus and caudate, in addition to cerebrospinal fluid, gray substance and white matter.

The clinical trial of Navarre:

A team of specialists from the University of Navarra Clinic has initiated a new clinical trial to curb the cognitive deterioration caused by Alzheimer's disease. This is a multicentric, recruitment-based investigation involving U.S. and European centers. Currently, about 600,000 people in Spain suffer from this disease.

The current treatment is aimed at people with a slight cognitive impairment, ie in the most incipient stages in which the disease still does not affect the day to day of the sick. However, this new drug (Crenezumab) also includes people with mild-stage dementia, that is, in those stages in which the patient begins to have problems in carrying out their daily activities.

As explained by Dr. Mario Riverol, neurologist at the University of Navarra Clinic, specializing in Alzheimer's disease and principal investigator in this essay: "These are antibodies that act on amyloid protein, which is deposited in the brain of the Alzheimer's, the main cause of the disease. The function of the drug is to "clean up" amyloid from the brain, in order to stop the evolution of the disease. "
The Alzheimer, which currently does not have a cure although there is treatment to lessen some symptoms, involves loss of memory, confusion and change of personality. Around the world more than 47 million people suffer from dementia, of which Alzheimer's disease is the most common form.

 

The new molecule that stops Alzheimer's:

A new molecule, called ASS234, stops the development of Alzheimer's disease and improves cognitive symptoms, as concluded a study with transgenic mice carriers of human genes treated to cause the disease, which has been carried out by Consejo Superior de Investigaciones Científicas(CSIC), the Universidad de Madrid and the Universitat Atònoma de Barcelona.

The characteristics of this molecule suggest its use to treat the cognitive deterioration and neurodegeneration underlying the Alzheimer. The study is published in the Journal of Psychiatry and Neuroscience magazine.

The effect of this new molecule is on the one hand that it blocks the aggregation or deposit in the brain of the toxic amyloid protein, implicated in Alzheimer's disease, and on the other, which stimulates the cholinergic and Monoaminérgica transmission, which improves Notably the cognitive symptoms of the disease.

The new ASS234 molecule, patented and developed by CSIC and UAB researchers, is designed as a hybrid of two known molecules. One is donepezil, which is currently used to treat cognitive deficits of Alzheimer, and the other is an inhibitor of the enzyme monoamine type B. This enzyme is activated in Alzheimer patients generating oxidative stress.

The study with mice that manages to stop Alzheimer's:

A team of researchers, led by the Spanish Magdalena Sastre, has developed a method to prevent Alzheimer's in mice by injecting a virus that allows to transmit a specific gene to the brain, according to a study published in Proceedings of The National Academy of Sciences.

This finding made by scientists at Imperial College in London, although it is in its early stages of research, could open the door to possible new treatments of the disease. Scientists consider that this gene, called PGC1-alpha, can prevent the formation of amyloid-beta péptida protein in cells in the laboratory.

This protein is the main component of amyloid plaques, a viscous mass of proteins found in the brain of people with Alzheimer's, and thought to trigger brain cell death.

This discovery can encourage new approaches to preventing or stopping the disease in its early stages. Although these findings are still very early, they suggest that this gene therapy may have potential therapeutic use for patients. There are still many obstacles to overcome, and currently the only way to transmit this gene is through direct injection into the brain.

The researchers injected the virus with the gene into two areas of the brain of mice where Alzheimer could develop, in the hippocampus (which controls short-term memory) and the cortex (which controls long-term memory), and are the first where Amyloid plaques begin.

The animals were treated in the first episodes of the disease, when they still do not have these plaques, and four months later it was found that the mice that had received the gene had very few of these plaques compared with the group of mice that had not been treated. Likewise, no loss of brain cells was recorded in the hippocampus.

Electroencephalogram to diagnose Alzheimer's:

Alzheimer is a neurodegenerative disease, that is, caused by the progressive destruction of brain neurons. A disease that is the most common type of dementia and currently has about 30 million people around the planet. It is more; According to the World Health Organization (WHO) estimates, the global number of people affected would rise to 53 million in just over three decades.

However, despite countless researches, no effective treatment has yet been discovered once the symptoms of the disease have appeared. Hence the crucial importance of early diagnosis of Alzheimer, which would enable better care and treatment of those affected since the initial stages of pathology. And in this context, researchers at the University of Birmingham (UK) seem to have given one of the keys to identifying those with a high risk of developing it: the deterioration in the processing of written language – or what is the same, the Loss of ability to identify or understand written words.

One of the main features of Alzheimer's disease is the progressive deterioration of language. However, there are very few studies that have investigated the language processing capacity during the period between the onset of the initial symptoms of the disease and its complete development».

To carry out the study, the authors counted with the participation of 25 elderly people who underwent an electroencephalogram – EEG, a test that analyses the electrical activity of the brain by means of electrodes placed in the head – to measure the time It took them to process the words they saw on a computer screen. Specifically, the sample of participants in the study included completely healthy older people, older with mild cognitive impairment, and patients who had developed Alzheimer's disease after being diagnosed less than three years ago from mild cognitive impairment.

The objective was to detect the possible existence of abnormalities in brain activity during language processing in patients with mild cognitive impairment, anomalies that could offer us a vision of their probability of developing Alzheimer. The reason why we focus on language is that it is a crucial aspect of cognition that is particularly deteriorated during the progression of the disease. '
In this context, previous research conducted with EEG has shown that the time required for a person's brain to process a written word is set at around 250 milliseconds. And the participants in this new study, did they meet these 250 milliseconds? Not really.

The most important result of our study is that the brain response is anomalous, if not ' aberrant ', in individuals who will end up developing Alzheimer's disease in the future. A response that, on the other hand, remains ' intact ' in patients who remain stable '.
The findings were totally unexpected, because although the language is affected in the Alzheimer, it occurs in much more advanced phases of the disease.

Identified the first drug to prevent the disease:

Around one million people in our country suffers Alzheimer, a neurodegenerative disease that affects 10% of the population over 65 years and for which there is no cure. However, the development of this disease could be prevented, and not only with the adoption of healthy living habits – in fact, the causes for which the disease originate remain unknown –. It could be enough with the administration of a simple drug. Or so it shows, at least, a study led by researchers from the University of Cambridge (UK) and published in the journal "Science advances".

The new research shows how a drug, called "Bexarotene" and already marketed for the treatment of cancer, is able to prevent the onset of Alzheimer's disease by stopping the first step of the cascade of reactions that cause the death of the Brain cells both in laboratory models and in studies carried out with nematodes – a type of worms.
As Michele Vendruscolo, director of the study, explains, "The organism has a variety of natural defenses to protect against the neurodegeneration. But as we age, these defenses deteriorate progressively and can be overcome. So, and understanding how these natural defenses work, we might be able to help them by using drugs that act in a similar way."

Amyloid beta in the human brain

The beta-amyloid protein performs numerous basic functions in the organism. The problem is that when they acquire an erroneous structure, these proteins adhere to each other forming amyloid beta fibers. A process called ' primary nucleation ' that continues with the binding of these fibers to form beta-amyloid oligomers – which in turn will form the beta-amyloid plaques –, in itself highly toxic to neurons and, according to many studies, Responsible for the death of brain cells that trigger Alzheimer's disease.
Therefore, in recent decades numerous studies have been developed to find a drug capable of destroying these oligomers. However, the results have been completely unsuccessful.

As Michele Vendruscolo points out, "if we want to block the aggregation of proteins we need to know exactly what's going on and when it's happening. And in this sense, we have developed a test that analyzes the process not just as a whole. It also allows us to know what happens at every stage of the process. And if we are able to stop the aggregation before it starts, then there will be no proliferation."