Mitochondrial Medicine in focus of Alzheimer research

Mitochondrial function of energy supply moves in Alzheimer’s research, more and more come to the fore. The previous therapy trials based on the approach to inhibit those affected the activity of the enzymes beta and gamma secretase and immunize sufferers against the A-beta protein. But the efforts brought no satisfactory results. From now on, the attention of researchers the mitochondria and its central role is to be obtained from the energy in the cells.

Mitochondrial Medicine: much more than just power plants of cells.

These small organelles are chaotically scattered in our cells. Each cell contains approximately 1500 mitochondria and where it is in the nerve cells even up to 5,000 of them. The rule is: the more energy needed an organ for its proper functioning then more mitochondria it needs. Are damaged mitochondria in their function, can be performance also like that organ after.

Over a mitochondrial disorder (so-called Mitochondriopathy) cells lose their mitochondrial gradually. What it means? That you are no longer the mitochondrial respiratory chain and mitochondrial DNA available. This causes the cells to die.

Another very important role of mitochondria, the control of the so-called. Programmed cell death (apoptosis). This is of central importance in a disease such as Cancer. The intact mitochondria ensure that the mutated cells are eliminated and will not compromise the healthy cells. In a mitochondrial this protective function of apoptosis can no longer be exercised, facilitating further pathological cellular activities.

Role of mitochondria in Alzheimer’s.

In Alzheimer’s disease there is a mass death of nerve cells The formation of new nerve cells (called neurogenesis.) Is suspended or no longer takes place. New synapses and axons cannot be produced in the brain enough.

The age is considered a central risk factor for Alzheimer’s disease. With the progressive aging processes reduced energy supply goes hand in hand in brain cells. The recent cell and animal studies have shown that the mitochondrial functions are just disturbed by aging and disease-specific proteins, such as tau protein and beta-amyloid.

These scientific observations form the basis for the new field of research on Alzheimer’s disease field. The decline in mitochondrial efficiency is a gradual process, which can lead to Alzheimer’s dementia with increasing age and other risk factors.

In the experiments carried out on animals, for example, was Ginkgo extract identified as an active ingredient, which may affect the mitochondria. According to the findings of the mitochondria-controlled cell death (apoptosis) and the formation of disease-specific enzyme beta-amyloid was inhibited and neurogenesis in the hippocampus is promoted.