Defective tau proteins

 Time is deceased was described for the first time in 1907 by the German psychiatrist Eloise as a timer. In performing histopathologic studies of the brain of his patient Augustine suffering from dementia he brought to light the presence of 2 types of lesions in the brain. Senile plaques and neurofibrillary tangles he reached the conclusion of a distinct disease of a cerebral cortex 100 years later, thanks to current scientific techniques research has made a great leap and the understanding of the disease. We know that the brain is made up of neurons and that these are interconnected to form a vast network. 

These connections known as synapses enable the transmission of information from one neuron to another. And now it's time for us to cease 10 to 15 years before the appearance of the symptoms to main lesions forms in the brain. Senile plaques composed of amyloid-beta protein and neurofibrillary tangles composed of tau protein. How is the senile plaque formed? On the surface of the neuron is a large protein called APP. Normally a PPS sectioned by enzymes on the surface of the neuron and it frees a protein called amyloid-beta. Amyloid beta-protein is then cleared in the body. In the case of Alzheimer's disease, there is an imbalance the amyloid-beta protein is no longer regulated and is found in greater quantity. The proteins assemble to form indissoluble fibrils can create senile plaques. Our New World February tangles formed. When a neuron communicates with another a signal goes from the body known as soma to the synapse to transfer the information. The signal passes through the skeleton of the neuron composed of microtubules. These micro 2 balls are stabilized by normal towel protein. And outsiders disease tau protein becomes defective and detached from the microtubules. Thus the skeleton of the neuron dissociates as it is no longer maintained. 

Defective tau proteins then assemble to form filaments in the neuron. Without the skeleton, the neurons degenerate and connections between the neurons are lost. The abnormal accumulation of tau filaments and the neuron creates neural February tangles and eventually causes the death of the neuron. How do the 2 lesions spread throughout the brain? Neurofibrillary tangles and senile plaques do not follow the same pathway in the brain over time. Neurofibrillary tangles first developed in the region called the hippocampus which is essential to memory and learning. They then reach the whole brain following a centrifugal movement. The process because it's a trophy that engenders global dysfunction. The progression of the lesions corresponds with the symptoms of the disease which began with memory problems followed by problems of language recognition and incapacity to perform gestures. Senile plaques develop differently there initially observed in the cortex secondly in the hippocampus and then the senile plaques reach the whole brain following a centripetal movement. Their progression does not correspond to the symptoms of the disease. But numerous questions remain unanswered we know that the presence of the 2 cerebral lesions is necessary to develop Alzheimer's disease since one does not come without the other. But which lesion comes first neurofibrillary tangle or senile plaque. The answer is still under debate. Many clinical trials destined to reduce senile plaques in the brain have failed in fact reducing them is not sufficient to eradicate the disease. It is now been suggested that well before the formation of senile plaques smaller forms of amyloid beta called Cali commerce appear to be toxic for neurons disturbing their communication when they fix on to synopsis. It would appear that the toxic oligomers and their accumulation of senile plaques are at the origin of neurofibrillary tangles which in their turn a responsible for symptoms. The relationship between amyloid-beta protein and tau protein is still little understood. 

What is the exact sequence of molecular mechanisms leading to the development of dementia? What is the role of genetics and environmental risk factors in the appearance of the disease? Scientific research is essential in answering these questions. Thanks to researchers house timers disease are better and better known in its complexity and new avenues raise real hope for the eradication of this devastating disease.