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Researchers are investigating Alzheimer’s with a new transgenic mouse model

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Researchers are investigating Alzheimer’s with a new transgenic mouse model

Researchers at the University of Illinois at Chicago College of Medicine are investigating the mechanisms underlying Alzheimer’s disease using a transgenic mouse model. The new model is actually a combination of the current model and a mouse that carries human apoE gene. ApoE4 is associated with an increased risk of developing Alzheimer. The new model faithfully mimics Alzheimer’s disease that occurs in humans and thus researchers can discover new therapeutic targets to treat disease as well as drugs to treat the disease.
UIC LaDu biochemist Mary Jo, who is associate professor of anatomy and cell biology at the UIC College of Medicine and principal investigator of the study, explained that beta-amyloid, a protein, is the main component of the plaques that are found in the brains of people who had Alzheimer’s. But before to form those visible plaques, beta-amyloid are grouped into smaller chains called oligomers. It seems that these oligomers are responsible for neurotoxicity.

Alzheimer's Disease

Alzheimer Disease

Although methods for detecting these oligomers are limited, researchers were able to create a monoclonal antibody to help identify these forms of beta-amyloid. LaDu noted that this monoclonal antibody helped to identify early accumulation of beta-amyloid and differences related to various forms of apoE4. ApoE4 may be a marker showing the risk of developing Alzheimer’s. The researchers noted that patients with apoE4  respond negatively to treatment in clinical trials.
Alzheimer’s disease is the most common form of dementia. It is expected that in 2050 one in 85 people will suffer from Alzheimer’s. There are two major forms of Alzheimer’s disease: early onset, which is rare, and it runs in the family, and late onset, which is the most common form. The most common symptoms are difficulty remembering recent events, confusion, irritability,  long-term memory loss. It is worth mentioning that once started, the disease has no cure as it is due to loss of neurons and synapses in the cerebral cortex.
There is no clear cause of Alzheimer’s disease, but there have been questioned several mechanisms. In some cases genetic factors play an important role. It seems that APP (amyloid precursor protein) mutation is responsible for the disease. This assumption applies especially for the early onset form. Other hypotheses were related to neurotransmitters in the brain. According to the cholinergic hypothesis, Alzheimer’s disease is due to the decrease of acetylcholine in the brain. Others believe that this disease is triggered by the accumulation of beta-amyloid in the brain. Others, however, believe that disease is caused by the accumulation of tau protein in neuronal bodies.