Alzheimer's disease is a progressive form of dementia characterized by the loss of memory and cognitive function. The loss of neural cells associated with Alzheimer's disease is believed to be caused by the accumulation of beta amyloid plaques and tangles inside neurons, notes the MayoClinic.com. Beta amyloid plaques and neurofibrillary tangles interfere with neural communication and function, eventually leading to the loss of neuron cells.
Beta Amyloid Plaques
Beta amyloid is small protein fragment produced from a larger protein known as amyloid precursor protein. The beta amyloid protein is naturally very sticky and can accumulate in densely coiled clusters known as plaques. According to the Alzheimer's Association, it is believed that a disruption in the formation, accumulation or removal of beta amyloid proteins is the primary cause of Alzheimer's disease. Researchers believe that the accumulation of beta amyloid plaques causes a disruption in neural communication and activates the inflammatory response by the immune system in which immune cells attack and further destroy neural cells.
Amyloid Precursor Protein
A mutation in the gene encoding the amyloid precursor protein is believed to be a causative hereditary agent. In normal brain cells, the amyloid precursor protein is processed by protein enzymes known as protease, which cut the protein into its active forms, A-beta40 and A-beta42. In Alzheimer's disease, mutations in the genetic information encoding amyloid precursor protein causes the protein to be cut incorrectly, thereby causing it to cluster or form amyloid plaques at a quicker rate as well as increasing the toxicity of the beta amyloid plaques. According to the University of Pennyslvania, mutations in the gene encoding the amyloid precursor proteins is a key part in the incorrect formation, accumulation or removal of beta amyloid plaques in hereditary Alzheimer's disease.
Apolipoprotein E
Apolipoprotein E is a protein that transports cholesterol and fat in the bloodstream. Apolipoprotein E interacts with beta amyloid proteins, influencing their deposition into plaques as well as neuronal repair efficiency. The gene encoding the apolipoprotein E protein determines which form of the apo E protein an individual will have. According to the Merck Manual, individuals with one form of the apolipoprotein are more likely to develop Alzheimer's, while those with another form are less likely to develop the disease.
