An Important Discovery:

Today we can find news that speak of the developments in the diagnosis and treatment of Alzheimer's disease. At the Hospital de la Santa Creu i Sant Pau in Barcelona made a series of tests and diagnoses in order to prevent Alzheimer's disease in its early stages:

- Have developed new techniques to diagnose the disease in early stages:

Until a few years ago, the only way to confirm that the patient had an excess of TAU protein or amyloid protein in the brain, which are involved in the disease, it was through an autopsy when he had died. Now, on the other hand, have developed techniques that allow you to detect the buildup of these proteins in people who still do not have any symptoms. It is one of the most important advances that have been made in recent years. One of these techniques is to perform neuroimaging tests; that is to make an MRI in patient of all your nervous system, and the other, in the analysis of cerebrospinal fluid, in which liquid is extracted from the lower part of the back part of the brain and which provide information relevant to detect absence, or not, of the protein.

Cerebrospinal fluid

MRI

- Researchers are developed many treatments to curb the disease:
There are different processes for example, clear the brain of excess of amyloid, to eliminate the deposits of protein TAU, to curb its occurrence or to combat inflammation of the brain. However, for the moment, none of these treatments has not been able to prove that significantly improves the symptoms. Although some of the tests that have been done are in advanced stages, still need a few years to find out if they have any real effect, these studies will need a very long time to finish from being carried out. All the experiments that have been carried out so far have not been positive. Although doctors don't even consider the possibility of setting up programs for early detection of Alzheimer's disease, can use these techniques to apply the treatments before, in patients with the disease in very initial phase, so it is possible that medications that until now had not had good results now have a different effect.

- They have discovered new genes linked to the disease:
In the last five years the researchers have identified a number of genes that are more common in people who suffer from Alzheimer's disease. These new genes, provide researchers with clues to figure out what are the mechanisms that can cause illness or some of their most common symptoms. Some of these genes, for example, might be linked with the brain inflammation that patients suffer in the initial stage. But not all of the people who have alterations in these genes will develop Alzheimer's disease. It only means that they can increase a little the chance of having it.

- It is known that a balanced diet and physical and mental exercise prevents the disease:

Researchers also confirmed last year in two studies that cardiovascular disease, such as hypertension, cholesterol or diabetes, are directly related to the onset of the disease. For this reason, doctors insist on maintaining a balanced diet and exercise regularly.

-The current studies are looking for ways to stop or cure the disease:

Treatments available today get a certain stability of the symptoms for a while, because they improve the connections between the neurons and the brain work best. This, unfortunately, does not slow down or prevent the disease, but at least improves the quality of life of patients for a long time. The latest treatment that was passed is from 2003. Since then, there has been no new approved drugs, because most focus to slow down or reverse the disease, a goal that, for now, the researchers have not reached.

100 million dollars to Alzheimer's disease:

The founder of Microsoft Bill Gates has decided to give 100 million dollars to the Fondo de Descubrimiento of Dementia in personal title.

The American Funds combined with the aim of addressing a

major global health problem and devote himself to the research

of treatments to alleviate the effects of the neurodegenerative disease.

The long research devoted to the disease have not managed to design a treatment effective braking of the devastating effects of Alzheimer's, which affects almost 50 million people around the world, a figure that is predicted will amount up to 131 million by in 2050, according to noted Alzheimer's Disease International. However, Gates is not pessimistic with regard to the future of science in this field.

REec & AEMPS:

El registre d'assaigs d'Espanya (REec) i l’Agencia Espanyola de Medicaments i Productes Sanitaris (AEMPS) are two web sites that aim to serve as a source of information for clinical studies with drugs of any kind of disease that can be treated . In this case, the disease of Alzheimer's are being carried out more than a hundred interventions in order to find a vaccine or a drug to slow or stop the disease. The two most frequent advances that are being made are:

-The ABvac40 vaccine:

The 23 of October of the same year, is carrying out a study to test a new vaccine called ABvac40 in order to be able to finish curing the disease of Alzheimer's, but specifically this shot can only be injected in patients who are in the first phase, that is to say, in the mild stage.
In this clinical trial participated 210 patients over the age of 64 years and of both sexes.
This multicenter study consisted of two separate groups, each cone were half of the patients, to whom he injected the vaccine contained in the medicine to cure the disease, and in the other group, with the other half of the patients , they were given the placebo.
At this time are still doing all the evidence and relevant observations and it is hoped that, within 24 months, doctors and researchers because they can get results to be able to present it to the market.
This vaccine is used with the aim of evaluating the safety and tolerance of repeated doses of the vaccine in a population of patients, evaluate the immune response, changes in vaccine induced biomarkers and evaluate the cognitive.

GRA@CE:

These years will be launched the project GR@ACE, the first study in Spain of genomic research on Alzheimer's in terms of number of samples of patients, more than 4,000, that will allow us to identify new genetic targets to treat this disease.   The project GR@ACE will be held for three years and has the momentum of "l'Obra Social la Caixa", which used the same 650,000 euros, and Grífols, with a contribution of 600,000 euros. The study is based on the application of genomic technologies of high resolution for the identification of a new generation of genes that provide data in the design of new treatments to tackle the disease. These data will be of great scientific and social value.

Up to now, the 99.6% of clinical trials of new drugs against Alzheimer's disease have failed. It is necessary, therefore, to find new ways in order to reverse the high current figures of this disease, which lead them to consider it and to the pandemic of the 21st century.
The project GR@ACE is part of a line of research a priority for Europe ("Programa Horitzó" 2020) and affects the form in the study of Alzheimer's disease, as it aims to integrative bioinformatics, personalized medicine and the identification of new therapeutic targets. One of the objectives of the study will be the selection of genetic targets for the treatment of Alzheimer's disease using bioinformatic techniques of positioning of drugs. From a strictly clinical point of view, the impact of genomic technologies for the diagnosis and the ability to predict will be of great importance, since, due to its high heritability, it is expected that the genetic characterization of patients with Alzheimer's to generate a change of model diagnosis in the future.

Washington found the key:

Researchers at the University of Washington and the St. Louis Medical School have found a key difference in the brains of people with Alzheimer's disease and those who are cognitively normal but still have brain plaques that characterize this type of dementia.

There is a very interesting group of people whose thinking and memory are normal, even late in life, however, their brains are full of beta amyloid plaques that seem to be identical to what is seen in Alzheimer's disease. We never understand exactly what causes dementia. Hard plaques made from a protein called amyloid beta are always present in the brain of a person diagnosed with Alzheimer's disease, according to Brody. However, the simple presence of plaques does not always result in impaired thinking and memory. In other words, plaques are necessary – but not enough – to cause Alzheimer's dementia. The new study, available online in the journal Annals of Neurology, is still assuming beta amyloid in the cause of Alzheimer's dementia, but not necessarily in plaque form. Instead, the small beta-amyloid molecules dissolved in the brain fluid seem more closely related to the fact that a person develops symptoms of dementia.

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."