Other research suggests that people with more years of formal education are less likely to develop Alzheimer’s. Some experts theorize that longer education may produce a denser network of synapses in the brain. Synapses are the nerve-fiber connections in the brain that enable neurons to communicate with one another.
A dense synapse network may create a kind of “neural reserve” that enables people to compensate longer for the early brain changes associated with Alzheimer’s. However, there could be other answers to this. Further research is required.
Early Life Experiences
Unsurprisingly, the environment in which a person lives Ã¢â‚¬â€œ especially early in life – has been implicated as a risk factor for many chronic adult diseases, including Alzheimer’s.
However, a recent study has linked a surprising selection of environmental, socio-economic, and early life experience factors to Alzheimer’s. For example :
An increased number of siblings was associated with increased risk of Alzheimer’s.
A rural residence in childhood, combined with fewer than six years of school, was associated with an increased risk for Alzheimer’s.
Growing up in the country, rather than in the suburbs, was associated with an increased risk for Alzheimer’s.
There is growing evidence that many of the well-established risk factors for cardiovascular disease, including high cholesterol and high blood pressure, may also be risk factors for Alzheimer’s disease.
Brain infracts, heart disease and mid-life hypertension increase the risk of AlzheimerÃ¢â‚¬â„¢s disease and Vascular dementia.
A large study by researchers in Finland supports this thinking. Among the study population of 1,449 people, elevated cholesterol and high blood pressure seemed to be even more strongly linked to the eventual development of Alzheimer’s than did carrying APOE-4 gene, the only known inherited risk-factor for the most common form of the disease.
Those people who carried the APOE-4 gene were twice as likely to develop Alzheimer’s than those with no genetic risk. However, if those APOE-4 carriers also had high blood pressure, then they were up to five times as likely to develop the disease.
When high cholesterol was also present, the risk jumped to eight times greater than those without APOE-4. This and a number of other studies around the world are strongly indicating that what’s good for the heart – keeping weight, cholesterol and blood pressure in check – may also be good for the brain.
One of the most alarming and controversial hypotheses about the potential risk factors for Alzheimer’s concerns aluminum, which became a suspect when researchers found traces of this metal in the brains of Alzheimer’s patients. This is indeed a grave concern because many people use aluminum pots and pans for cooking, and aluminum canteens for drinking in the world.
Many studies since then have either not been able to confirm this finding or have had questionable results. Aluminum does turn up in higher amounts than normal in some autopsy studies of Alzheimer’s patients, but this certainly doesn’t occur in all. In addition, the aluminum found in some studies may have come from substances used in the laboratory to study the brain tissue after death. Moreover, various other studies have found that groups of people exposed to high levels of aluminum do not have an increased risk of developing Alzheimer’s. On the whole, scientists can say that it is still very debatable whether exposure to aluminum plays any role in the development of Alzheimer’s disease.
Zinc has been implicated in Alzheimer’s disease in various studies. Some research reports suggest that too little zinc may be a problem, while other studies suggest that too much zinc is an issue.
There is a growing pool of evidence that suggests that what you eat is very important to your brain. A range of recent studies have reported a link between dietary habits and specific nutritional factors to the risk for Alzheimer’s disease and/or cognitive decline.
In particular, the benefits to the brain of a low-fat diet rich in antioxidants such as vitamins E and C throughout life are becoming clearer.
Here’s what some of the latest research studies have found :
A diet rich in foods containing vitamin E may help protect against Alzheimer’s in some people, according to a study conducted at Rush-Presbyterian-St. Luke’s Medical Center in Chicago and reported in the prestigious Journal of the American Medical Association (JAMA).
Such foods include vegetable oils, nuts, green leafy vegetables, and whole grains. Furthermore, the protective effect was NOT seen when study participants took vitamin E supplements, as opposed to getting more of the vitamin from foods. The most significant protective effect was found among those who had the highest dietary intake of vitamin E (which averaged 11.5 International Units per day); their risk of developing Alzheimer’s was 67 percent lower than people who consumed the least amount of vitamin E from food sources.
As a person ages, their brain undergoes a number of changes :
Some nerve cells, called neurons, in various regions of the brain die, although the neurons most important to learning usually live on.
Some neurons, and the fibers that connect them to other neurons, shrink and degenerate. This tends to especially occur areas of the brain that are important to learning, memory, planning, problem solving, and other complex mental activities.
Twisted fibers, called tangles, develop within neurons and protein plaques develop in the areas surrounding neurons.
Tiny structures inside neurons that metabolize energy for cell functions become more susceptible to damage. Inflammation (swelling) of the brain increases, which cause damage to nerve cells.
Oxidative stress increases. This is caused by the release of special molecules, called free radicals, from normal cellular processes. This can lead to nerve cell damage and death.
In healthy older people, the impact of these changes may be modest, resulting in various degrees of age-related memory decline. In people who have Alzheimer’s, however, some of these changes are much more extreme, with devastating consequences. Det
Sporadic Alzheimer’s, also known as Late Onset Alzheimer’s, is the most common form of Alzheimer’s by far, and tends to occur much later in life than FAD. That is, it can affect adults of any age, but it usually occurs after age 65. This form Alzheimer’s can affect people who may or may not have a family history of the disease. There is currently no evidence that autosomal dominant inheritance of mutated genes causes Sporadic or Late Onset Alzheimer’s. However, genetics does appear to play a significant role in the development of this far more common form of the disease.
Different variations, or alleles, of particular genes produce variations in inherited characteristics, such as height, skin color, eye color, blood type, and so on. In the early 1990s, researchers at Duke University in Durham, North Carolina, found an increased risk for late-onset Alzheimer’s in people who inherited one or two copies of a particular variation of a gene called apolipoprotein E (APOE) – the variation known as APOE e4.
Apolipoprotein E is a protein that has various functions, such as helping the blood to carry cholesterol throughout the body.
Familial Alzheimer’s Disease (FAD) is a very rare form of AlzheimerÃ¢â‚¬â„¢s, and runs in very few families. If a parent has a specific mutated gene, then any children have a 50% chance of inheriting and developing the disease. The presence of the specific mutated gene means that the person will eventually develop AlzheimerÃ¢â‚¬â„¢s disease, usually in their 40Ã¢â‚¬â„¢s or 50Ã¢â‚¬â„¢s.
This form of AlzheimerÃ¢â‚¬â„¢s affects a very small number of people. The total known number of FAD cases worldwide is about 200 people. All instances of FAD that have been studied so far have a much earlier onset, and as many as 50 percent of FAD cases are now known to be caused by defects in one or more of three genes located on three different chromosomes inside the person’s cells:
1.Amyloid Precursor Protein (APP) Mutation: Some families have mutations in a gene called amyloid precursor protein (APP), which causes an abnormal form of the amyloid protein to be produced.
2.Presenilin 1 Mutation: Other families have mutations in a gene called presenilin 1, which causes an abnormal presenilin 1 protein to be produced.
3.Presenilin 2 Mutation: Presenilin 2 is a gene very similar to presenilin 1, and when this gene is mutated, then it causes an abnormal presenilin 2 protein to be produced.
It is highly likely that the Alzheimer’s results from a complex and interrelated combination of genetic and non-genetic factors.
These so called risk factors influence a person’s risk to developing Alzheimer’s disease. Currently, each of these risk factors is the subject of a great deal of research around the world.
Genetic Risk Factors
A person’s genetic make up can directly influence the chances for the onset and development of Alzheimer’s. A person’s genes are inherited from their biological parents and passed along family lines to their biological children.
There are two main types of Alzheimer’s Disease.
Familial Alzheimer’s Disease (FAD): is a very rare form of Alzheimer’s Disease which runs in families. Also known as Early Onset Alzheimer’s or Younger Onset Alzheimer’s.
Sporadic Alzheimer’s Disease: is the most common form of Alzheimer’s Disease, but researchers are still trying to work out how this develops. Also known as Late Onset Alzheimer’s.