Genes that promote Alzheimer's

Alzheimer’s disease is a neurodegenerative disease, associated with improper protein folding, which leads to mental impairment and finally death. The disease arises as a consequence of the misfolding and subsequent clumping together or aggregation of abnormal Beta proteins, and the formation of a toxic misfolded protein in the body. The basic physical properties of a protein molecule may differ and how a protein is able to fold into a stable three-dimensional shape, which can adversely affect the correct formation of properly functioning proteins. The correct three-dimensional structure is essential to function, although some parts of functional proteins may remain unfolded. Failure to fold into the intended shape usually produces inactive proteins with different properties including toxic prions. Several neurodegenerative and other diseases are believed to result from the accumulation of misfolded (incorrectly folded) proteins, such as Alzheimer’s. Rather than becoming present due to an invading infection of the body by a virus or a bacterium, these diseases are of the body's own making. Alzheimer's disease is often referred to as “protein misfolding disorder”. This disease it thought to be genetically induced. This may be due to an APOE ε4 allele, which is most highly associated with Alzheimer’s for individuals with a family history of dementia, and this association is highest for individuals that carry 2 APOE ε4 alleles (ε4/ε4 genotypes). There is not cure for AD at the moment. This means that treatments will only manage to slow down the progression of Alzheimer’s in some patients. There are though to be three genes responsible for the early onset of the disease, which are APP, PSEN1, and PSEN2. This means that Alzheimer’s is becoming more prevalent in younger generation with multiple gene responsible for the disease. In the past only on gene, the APOE gene, which is normally associated with people who are 60 years of age and on. There are several studies where this APOE gene has been studied and it is still unclear why these proteins function in an improper manner. At present, there is no definitive evidence to support that any particular measure is effective in preventing Alzheimer’s. Global studies of measures to prevent or delay the onset of Alzheimer’s have often produced inconsistent results. However, epidemiological studies have proposed relationships between certain modifiable factors, such as diet, cardiovascular risk, pharmaceutical products, or intellectual activities among others, and a population's likelihood of developing Alzheimer’s. Only further research, including clinical trials, will reveal whether these factors can help to prevent Alzheimer’s.

Hanna Martin