The most usual case of dementia is Alzheimer’s disease. The expression dementia designates a lot of symptoms that can include memory loss and difficulties with thinking, problem-solving or oral communication. These symptoms happen when the brain is damaged by certain diseases, including Alzheimer’s disease. During this condition, proteins build up in the brain to form structures called ‘plaques’ and ‘tangles’, which contributes to the loss of connections between nerve cells, and eventually to the destruction of nerve cells and loss of brain tissue.
A lot of the research examining the causes of dementia has focused on Apolipoprotein E (ApoE), which in certain genetic forms can support the buildup of toxic amyloid plaques in the brains of Alzheimer’s patients. Researchers at the Institute’s Center for Translational Neurodegeneration Research and elsewhere are trying to determine whether reducing ApoE in the brain could finally be a feasible therapeutic alternative for treating Alzheimer’s.
The retrospective study examines how various bodily systems fail due to ApoE, which, among other functions is responsible for transporting and filtering b-amyloid, the toxic substance that accumulates in Alzheimer’s disease.
The type of ApoE produced by the ApoE gene determines how effectively amyloid is removed from the brain. ApoE2 is the most effective, ApoE3 is in the middle and ApoE4 is the least efficient and therefore most likely to allow the buildup of amyloid plaques. People whose genes produce ApoE4 are at high hazard of getting Alzheimer’s, according to the review compiled by Center Director Dr. Joachim Herz, Professor of Molecular Genetics, Neuroscience, and Neurology and Neurotherapeutics, and Courtney Lane-Donovan, a Medical Science Training Program student.