Researchers reveal a possible cause of "Alzheimer"

An international research team from the “French Health and Research Institute” in collaboration with French “Bordeaux University” and the Canadian University of Moncton has managed to prove a direct causal link between the disorder of the mitochondria activity and the rise of cognitive symptoms associated with neurological degenerative diseases such as “Alzheimer’s”. Mitochondria is often known as “power plants” in the cell, where it plays an important role in the survival of living organisms, and is responsible for generating the majority of the cell supply of adenosine tribes that are considered the basic currency of energy in the cell, and is used to operate all cellular activities. The energy production process within the mitochondria takes place through the cellular respiration process, as it converts glucose and other nutrients into useful energy. The mitochondria consist of an outer membrane around it, and an involuntary internal membrane increases the area to improve adenosine threefold phosphate production. In addition to its energy role, Mitochondria has other important functions, including regulating the death of the programmed cells known as ‘Samatic’, Calcium and Temperature Production. The mitochondria inherit only from the mother, whereby scientists detect the maternal genealogies. Any imbalance in mitochondria can lead to a wide range of diseases, such as cardiovascular disease and diabetes. In the study published in the journal “Nature Neuroscience”, the researchers relied on the development of an innovative instrument called Mitodreadd -GS, an industrial future that can activate the “G” proteins directly within the mitochondria, which stimulates energy production in neurons. This tool was developed with the aim of controlling the activity of mitochondria, and this instrument is characterized by the ability to specifically target mitochondria by directing it to communicate with the G proteins in the mitochondria. The idea of this instrument depends on the fact that the associated G -acre protein receptors, which are important receptors in the brain, can also be present on the membranes of mitochondria, as it directly affects the production of cellular energy. The first proof of its kind and when this technique is applied to mouse models with dementia symptoms is a clear improvement in memory functions and the return of mitochondele activity to its normal levels. According to the research team, this improvement indicates that the decline in the activity of mitochondria can precede the loss of neurons, which changes the prevailing view that is considered the mitochonde dex, only a later consequence of the disease and opens the door for Mitochondria as a possible new treatment goal. The lead author of the study, Giovanni Marikano, said that the study for the first time proves the existence of a causal relationship between the Mitochondria defect and the symptoms of neurological degenerative diseases, which supports the idea that the imbalance in energy production may be the initial engine to begin the neurons. According to the study, when the ability of mitochondria to weaken energy, the effectiveness of receiving neuro transfer in nervous conflicts of conflict – nerve trips – decreases, so start to weaken and memory begins to weaken and cognitive performance begins to deteriorate. This energy shortage is not a simple problem; This can be the first spark of a broader range of cellular imbalance. What are neurological degenerative diseases? Diseases that affect the brain and lead to the death of nerve cells and shrink the size of the brain. It occurs due to a defect in communication between the brain cells, leading to their collapse and death. These diseases affect many important functions such as movement, memory, speech and intelligence. The causes of most of these diseases are still unknown because of their complexity. Examples of neurological degenerative diseases: Parkinson’s disease (Parkinson’s): It is related to problems in motion and occurs as a result of the death of neurons in the black dust area in the brain, which produces the necessary dopamine fabric to communicate with the basal nodes responsible for movement and leads to trouble in starting movements, tremors and stumbling. Huntington’s disease: a genetic disease that is transmitted from parents to the children and affects the basal nodes and causes an abnormal accumulation of protein, leading to the death of neurons and involuntary and excessive movements, such as limbs. Death: A general term indicates memory loss and the most famous species of Alzheimer’s disease and Lii particles and occurs as a result of the death of a large number of neurons in different areas of the brain, leading to memory loss and problems with thinking and movement. Treatment and future hope are currently no healing treatment for these diseases, and scientists develop the idea of using stem cells – which are immature cells that can switch to any type of cells, including neurons – to replace dead neurons. Challenges: Despite the success of animal experiments, there are still major challenges to apply this technique safely to people, such as building structures that support the growth of stem cells in the brain. The sick mitochondria tend to produce more oxidized interactive particles, known as free radicals that cause fats, proteins and DNA within cells. The damage of the components of the membrane and protein directly affects the transmission of signals and the structure of neurons, and contributes to the formation of mutual or distorted proteins known as they are associated with diseases such as Alzheimer’s and Parkinson. Mitochondria also plays a fundamental role in organizing calcium ions in the cell, especially in nervous contact points. And if the mitochondria lose its ability to properly absorb and store calcium, the calcium concentration is increasing within the cells, leading to excessive cell alarm and stimulating paths leading to programmed death. The mitochondria are also not stuck, it is subject to division and integration, as it is transferred along the nerve axles to feed the ends of the distant nerve station, and if the balance of division and integration collapses, or the cellular transport mechanisms are disrupted, the mitochondrias become small or not at the places where the cells need more; The peripheral clamps are deprived of energy and the collapse of local jobs, which gradually contribute to a wide network insufficiency and a local cell death. Elastic evidence and natural cells get rid of damaged mitochondrias by internal cleaning mechanisms, and if this system fails, damaged orgasms collect less energy and loosen toxins in the cell and increase the accumulation of mitochondria oxidant pregnancy and increase a local inflammatory response in the brain, such as supporting cells – and change the nerve. is harmful to the nerve transport. The researchers said that the DNA in the mitochondria is vulnerable to damage with age, and the accumulation of mutations or damage to this DNA affects the electron exporting molecules responsible for energy production, which leads to chronic lack of providing cells and the palaces over the years to weaken the functional reserve of neurons. The evidence has long been overlapped between the fact that the Mitochondria defect as a result of the disease or one of its causes. But modern animal experiences reformed the image, after the experiments succeeded in increasing the effectiveness of the mitochondria by cleaning it, causing an improvement in memory and behavioral functions in animal models for neurological degeneration diseases. These results are not determined after a therapeutic effectiveness on humans, but it reinforces the hypothesis that a defect in the mitochondria can be a direct cause of the course of the disease, and not just a subsequent sign. In the future, the co -author of the study, Etienne Hippere Sheatin, a researcher at the University of Moncton, said that in the future the instrument could help detect molecular and cellular mechanisms responsible for dementia, which pave the way for more effective treatment orientation, and that the work will continue to see the effect of the continuous stimulation of Mitechondria Neurons can occur. The researchers added that the practical result of this study lies in the knowledge that Mitochondria is a promising therapeutic purpose, either by improving energy production, improving the cleaning of damaged organs, or even adjusting the dynamism of division and integration, or protecting mitochondria from oxidative stress. However, the researchers said: “We need to be careful, because the diseases of nervous degeneration are multiple and complicated, and which are correct in a laboratory mouse, may not be transferred to people automatically. The research is promising, but it needs close human studies before talking about practical and comprehensive treatments.”