Its Official Women Are More Prone Than Men in Developing Alzheimer's Disease

There are one hundred billion nerve cells (neurons) within our brain connecting to the many forms of communication networks of the body. Several groups of nerve cells have specific functions, such as thinking, remembering, and learning. Other groups help us to smell, see and hear.

Imagine the brain as a factory at work almost twenty-four hours a day, receiving supplies, generating energy, constructing things and waste removal. Then there is the process and storing of information and the main communicating with the other nerve cells. The work function keeps everything moving perfect, but it does require co-ordination and oxygen.

Researchers have discovered plaques and tangles, two abnormal structures which are the prime suspect for causing damage and killing nerve cells within the brain. Plaques are deposits of a protein fragment called beta-amyloid that builds up in the spaces between nerve cells are referred to as plaques, and Tangles are bent fibres of another protein called tau that tend to build up inside of the cells.

As people age, they develop some plagues and tangles and those diagnosed with Alzheimer's are found to generate far more. Recent study has shown that the plagues and tangles are developed in a conventional method and expand in areas critical to memory before dispersing into other areas of the brain. It is not sure what roles these two abnormal structures exactly have but scientist believe they play a vital role in closing the connections among nerve cells and disturbing the procedure that cells need to survive.

With every moving and working nerve cell running well, and when an unexpected failure occurs in the process an onslaught of problems can occur. Scientists believe microscopic changes in the brain appear long before Alzheimer's illness prevents part of the cells from functioning properly. The damage and death of nerve cells are the main course of memory malfunction and other dementia symptoms of Alzheimer's disease.

They are not sure where the trouble starts and ongoing research will help us to learn more about this disease. As the damage spreads, cells begin to lose their ability to work well and eventually die causing irreversible changes in the brain.

A recent study had concluded that women develop symptoms of Alzheimer's disease at a faster rate than men do. A study conducted on Alzheimer's sufferers of both sexes found that men with the problem regularly outperform women on tests that measured a senior's memory capacity and their ability to perform verbal, distance and depth tasks.

Research indicates that women are more likely to be diagnosed with Alzheimer's disease than men are and the investigation into this research has been sparse and inconsistent. This present study aimed to get a clearer understanding of gender based differences and the possible causes of these disparities.

Several indications research has seen the cause of some of the disadvantages of women contracting the disease than men. Hormones play an enormous role in making women more susceptible to Alzheimer's and studies have shown that estrogen may serve as a shield against the disease.

Men have proved to be more powerful and have cognitive reserves, which prove as a buffer against the symptoms of Alzheimer's, and other forms of dementia. It appears that men have more exposure to reserve building activities than women do.

Another factor considered are the genes and the primary genetic risk factor for Alzheimer's disease, the APOE genotype has proved to be more damaging on the cognitive functioning of women than men.

Alzheimer's is at the forefront of biomedical research today, and many possible approaches are currently investigated worldwide. Researchers are uncovering many aspects of the disease and related dementias as possible. Some of the most remarkable progress has shed light on how Alzheimer's affects the brain. A better understanding of how this works will lead to improved ways of dealing with this disease.

This article was published on the Guardian LV a while back.