Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by loss of cognitive function and changes in brain structure. One of the hallmarks of AD is the accumulation of amyloid-β (Aβ) plaques in the brain. Aβ is a peptide that is produced by the cleavage of amyloid precursor protein (APP). APP is a transmembrane protein that is expressed in many tissues, including the brain.
The role of genomic changes in specific brain cells in AD is not fully understood. However, it is known that APP is cleaved by two enzymes, β-secretase and γ-secretase. Mutations in the genes encoding these enzymes have been linked to early-onset familial AD.
APP is also cleaved by α-secretase, which prevents the formation of Aβ. The gene encoding α-secretase is located on chromosome 21. Down syndrome (DS), which is caused by the presence of an extra copy of chromosome 21, is associated with an increased risk of developing AD. This suggest that changes in the α-secretase gene may play a role in the development of AD.
It is also known that the levels of Aβ in the brain are regulated by the liver. This suggests that changes in the genes encoding proteins involved in liver function may also play a role in AD.
There is still much that is unknown about the role of genomic changes in AD. However, the Identification of these changes may provide insight into the development of this disease and lead to the development of new treatments.
The cells most affected by Alzheimer’s disease are the neurons in the brain. The main function of neurons is to transmit messages throughout the nervous system. In Alzheimer’s disease, there are characteristic changes that occur in the neurons in the brain. These changes are caused by alterations in the DNA.
The changes in the DNA can result in the overproduction of a protein called amyloid-beta. This protein is a normal component of neurons, but in Alzheimer’s disease, there is an excess of this protein. The amyloid-beta protein can build up in the neurons and form clumps called plaques. The plaques can damage and kill the neurons.
Another DNA change that can occur in Alzheimer’s disease is the overproduction of tau protein. Tau is another normal protein found in neurons. In Alzheimer’s disease, the tau protein can form tangles within the neurons. The tangles can damage the neurons and prevent them from functioning properly.
The changes in the DNA that lead to the overproduction of amyloid-beta and tau proteins are thought to be important factors in the development of Alzheimer’s disease.