Continuing with an article published by the Harvard Health Publications on the causes of memory impairment.

Genes
Dozens of studies — involving more than 10,000 pairs of twins — have shown that genetic differences account for about half of the variation in people’s mental abilities. Your genetic makeup also affects the degree to which you experience age-related memory loss and your risk for conditions that can impair memory, such as high blood pressure and Alzheimer’s disease. If your parents or older siblings have memory loss, you are at higher risk than others who do not have this problem in their families.
Scientists have identified a common genetic variant that impairs memory. Normally, the gene directs the production of a chemical called brain-derived neurotropic factor, which travels to the synapses and regulates memory. However, the gene’s so-called met variant, which is inherited by one-third of all people, encodes for a variant of this chemical. The result is that the chemical doesn’t reach the synapses effectively. In one study, people who inherited one or two copies of the met variant did not do nearly as well on a memory test as people who inherited two normal copies of the gene. The brains of these people also appeared to function differently: functional MRI images revealed that people with this gene variant had a different pattern of activity in the hippocampus than did other people.
Genetic factors are clearly relevant for families with a history of early-onset Alzheimer’s. This rare form of the illness, which accounts for less than 1% of all Alzheimer’s disease cases, typically appears before age 50. It is caused by abnormalities in three genes, all of which increase the production of beta-amyloid, which is deposited in the plaques found in Alzheimer’s.
However, one form (or allele) of a gene that directs the manufacture of a protein called apolipoprotein E (Apo E) has been linked to the more common late-onset Alzheimer’s disease. In particular, inheriting the APOE4 gene variation increases your chances of getting the disorder when you are older.
In 2007, researchers uncovered another gene that appears to contribute to Alzheimer’s-related brain changes. Their study, described in Nature Genetics , linked variations in a gene known as SORL1 to the formation of amyloid plaques in the brain. Using blood samples from 6,000 people in North America, Europe, and Asia, scientists isolated the SORL1 variation by looking at the genetic profiles of families in which two or more members have Alzheimer’s disease. When they compared blood samples of people with and without Alzheimer’s, researchers found that the people with the disease had less than half the level of SORL1 protein as did non-affected individuals.

Lessons from the Nun Study
In 1986, a young epidemiologist named David Snowdon engaged a community of 678 retired Catholic sisters in Minnesota in his research on healthy aging. This marked the beginning of an ongoing research project known as the Nun Study, which has yielded groundbreaking insights into the hows and whys of Alzheimer’s disease. The unprecedented wealth of information available about the sisters’ personal and medical histories, combined with the relative uniformity of their lifestyles, allowed researchers to tease out the medical and social factors that put an individual at risk for developing dementia.
One of the most significant findings has been the understanding of how cardiovascular factors interact with Alzheimer’s disease pathology. The women in the study who seemed to fare the best cognitively were those whose brains showed little evidence of stroke, even if they had brain damage consistent with moderate to advanced Alzheimer’s. From this, researchers conclude that a healthy brain has reserve capacity it can draw on to maintain normal functions even when Alzheimer’s disease is present. On the other hand, when the brain is compromised by cardiovascular disease, dementia symptoms appear at an earlier stage (see “Cognitive reserve: Engage your brain”).

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