Alterations and stages in alzheimer diseases: A review

We know the brain is made up of Neuron and these are interconnected to form vast network, these connections are synapse and able to transmission of information from one neuron to another. In AD 10 to 15 years before the appearance of symptoms two main lesions form inthe brain senile plaques composed of Amiloid â protein and Neurofibrillary tangles composed of tau protein On the surface of neuron a large protein called APP, normally APP is sanctioned by enzyme on the surface of the neuron and it freeze a protein called amiloid â .The amiloid â protein then cleard in the body and in case of AD there is an imbalance .The amiloid â protein no longer regulated and found in too greater quantity. The numerous question remains unanswered we know the presence of two cerebral leason is necessary to develop AD,since one will not come with other which leason comes first NFT or senile plaques the answer is still under debate Many CT are destined to reduce senile plaques in the brain have failed .In fact reducing them is not sufficient to eradicate the diseases. It is now been suggested that well formation of senile plaques smaller form of amiloid â called oligomer appeared to be toxic to neuron, disturbing that communication when they fix on synapse it would appear that the toxic oligomer and their accumulation senile plaques or at the origin of NFT which is in their turn are responsible for symptoms. The relationship between amiloid â protein and tau protein still little understood. what is the exact sequence of molecular mechanism and lead in to development of dementia .what is the role of genetic and environmental risk factor in the appearance of diseases. Scientific research is essential and answering these question .Thanks to researcher AD is better and better known in its complexity and new avenue raise real hope to eradicating this devastating diseases.