The results of a new study published in the journal Neurobiology of Aging suggest that the pathological forms of two proteins, beta-amyloid and tau protein, which are signs of brain pathology in Alzheimer's disease - plaques and neurofibrillary tangles - can act in tandem, damaging the mitochondria and Reducing the survival of neurons, according to an online edition for girls and women from 14 to 35 years old Pannochka. Net These findings are part of the results of several laboratories that are of particular importance in the development of a variety of brain diseases, including Huntington's, Alzheimer's and Parkinson's diseases, attach to cellular components known as mitochondria.

Mitochondria - tiny power stations inside neurons and other cells - are constantly in motion, producing a large amount of energy that cells use to live. In addition to energy mitochondria, other functions are performed, for example, such as maintaining a normal level of calcium in the cell. A cell with damaged mitochondria is unable to produce enough energy to sustain its vital activity, can not maintain the necessary levels of calcium and produces an increased amount of damaging oxidant molecules. Such events can occur in the brain in Alzheimer's disease, leading to the inability of neurons to function properly.

"Over the years, the idea that beta amyloid and tau protein work together, harming the brain, is increasingly spreading among scientists," says Gael Johnson, a professor of anesthesiology, PhD, principal author of the article. "The exact relationship between the two pathologies is unclear, but when Alzheimer's disease comes to their effect on mitochondria, synergy can manifest itself".

Professor Johnson's group paid particular attention to the pathological form of tau protein, which normally helps stabilize the neuronal transport network, called microtubules. In recent years, scientists such as Professor Johnson have been focusing on studying the abnormally short form of this protein, known as truncated or processed, tau, as one of the possible candidates for a role in the development of Alzheimer's disease.

Professor Johnson's team examined the performance of mitochondria of neurons in rats exposed to beta-amyloid, a conventional tau protein, a processed tau variant and a combination of beta-amyloid and two tau variants. In one experiment, scientists tracked the movement of mitochondria through neurons, taking pictures every 10 seconds during a five-minute period.

The most significant changes in mitochondria were observed when beta-amyloid and processed tau were present in the cell together. In this case, the mitochondria had only a third of the electrical potential compared to the control. Mitochondria are usually extremely mobile and distributed throughout the cell. However, in the presence of truncated tau and beta-amyloid, they abnormally coalesced in some parts of the neurons and could not enter the synapses, as is normal. In general, only about half of the mitochondria retained their mobility compared to cells not exposed to pathological proteins. Cells exposed to processed tau and beta-amyloid were less able than usual to respond to cellular stress. The number of reactive oxygen species, or free radicals, in such cells is increased by 60 percent. The mitochondria were fragmented, and their average length was only half the normal organelles.

Changes in neurons probably occur earlier than the patient begins to experience symptoms such as memory loss. Most scientists believe that changes in the brains of patients with Alzheimer's disease begin for years or even decades earlier than the signs of the disease become apparent.

"By the time the cells are dead, it's too late to do anything," says Professor Johnson. "Therefore, in the field of research on Alzheimer's disease, scientists are looking for early markers and indicators of the disease so that patients can be identified before the massive death of nerve cells. In addition, many laboratories are searching for treatment methods aimed at these early events ".

Perhaps, adds Professor Johnson, new information on mitochondrial dysfunction in Alzheimer's disease can be used to combat it, since this is probably an important target for therapeutic intervention. Given that Alzheimer's is a very complex disease, the monotherapeutic approach may not be as effective as a combined therapeutic strategy, as it is in the treatment of other diseases, including cancer and diabetes. To develop effective treatment methods that can improve the functions of mitochondria and neurons, further research is needed on how and why mitochondria are damaged in Alzheimer's and other neurodegenerative diseases ".

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