Fixing Genetic Risk of Alzheimer’s disease
Alzheimer’s disease is the most widespread disease of a large class of disorders which clinically are known as “dementias”, they are diseases characterized by a progressive deterioration of thinking ability and of memory. Alzheimer’s is a disease of the brain, in which nerve cells die and their connections with other nerve cells are lost. 1 People who have Alzheimer’s disease have set of symptoms that can include memory loss and difficulties with thinking, problem-solving or language disturbance the cause of the disease is stated to be unknown although, many scientists believe accumulation of the protein amyloid in the brain that leads to nerve cell death is the main cause. However, it appears that many risk factors also play a role in the disease like increase age, high cholesterol levels, high blood pressure and genetics less than 5% of people develop the disease in the fourth or fifth decade of life (40s or 50s). At least half of these early onset patients have inherited gene mutations associated with their Alzheimer's disease like apoE4. Moreover, the children of a patient with early onset Alzheimer's disease who has one of these gene mutations has a 50% risk of developing Alzheimer's disease. The aim of this report to see a potential solution for the primary genetic risk factor (APOE4) for Alzheimer's disease
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Alzheimer’s is a disease of the brain, in which nerve cells die and their connections with other nerve cells are lost. People who have Alzheimer’s disease have set of symptoms that can include memory loss and difficulties with thinking, problem-solving or language disturbance many scientists believe accumulation of the protein amyloid in the brain that leads to nerve cell death is the main cause. However, it appears that many risk factors also play a role in the disease like increase age, high cholesterol levels, high blood pressure and genetics like APOE4 mutation now in a new study published in Nature Medicine, researchers revealed how apoE4 confers its risk for Alzheimer’s disease in human brain cells. They were able to erase the damage caused by apoE4 by changing it, with a small molecule, into a harmless apoE3-like version. They tested on human cells because mouse models failed in clinical trials they can’t mimic the human disease by creating neurons from skin cells donated by AD patients and confirmed that apoE4 does, indeed, cause damage in human cells finally, the researchers looked for ways to repair the abnormalities caused by apoE4. In earlier work, they developed a class of compounds that can change the structure of the harmful apoE4 protein so it resembles the innocuous apoE3 protein, referred to as apoE4 “structure correctors However still the scientist are working to improve the compounds so they can be tested in human patients in the future
