Researchers have discovered that people whose brains display thinning of the cerebral cortex are at significantly higher risk for developing Alzheimer’s disease, even if they are currently cognitively healthy.
It is estimated that 15 million people in the United States suffer from the disease and that caregivers spend an unpaid 17 billion hours alleviating its devastating symptoms.
Alzheimer’s is a rapidly progressing form of neurodegenerative senile dementia that often presents itself in old age. Family members typically sense confusion, irritability and forgetfulness in the elderly, resulting in a less-than-hopeful prognosis. However, researchers have recently found that the thinning of key cortical areas in the brain may predict Alzheimer’s up to a decade before symptoms begin.
Neurologists have long known the characteristic signs of Alzheimer’s from MRI analysis. The appearance of certain plaques indicates areas of neurodegeneration in the brain. There may be a genetic influence as well; sequences on chromosome 21 as well as the apoE gene have been linked to Alzheimer’s.
However, most cases of the disease are sporadic, meaning that they do not have an ascertained familial inheritance. It is now known that proteins do not fold properly in patients with Alzheimer’s disease. Alpha, gamma and tau proteins misfold and accumulate in the brain. These misfoldings result in the plaques seen on the scans.
In the study, patients in their 70s with similar educational backgrounds participated in long-term observation of brain changes. The patients were given memory tests and several MRI scans over the course of several years. Some participants were judged to be cognitively normal at the outset of the study while others had already begun to show initial signs of Alzheimer’s.
After nine years, all patients diagnosed with the disease had a thinning of the cerebral cortex in areas known to be most vulnerable to the plaques characteristic of Alzheimer’s. Those who had suffered the most significant thinning also presented the worst symptoms of the disease.
Patients who had started with relatively thin cortical areas developed the disease more rapidly than patients with a normal thickness. In the group with thin cortical areas, 55 percent of patients developed dementia during the study while only 20 percent showed signs of lost cognitive function in the normal group. Statistically, patients who had one standard deviation of thinning below the average thickness were those who suffered from a more rapid onset of symptoms.
This study is crucial to Alzheimer’s research because it provides hope for predicting the disease before its onset. Alzheimer’s worsens with time, and late stage patients are entirely dependent on their caregivers for survival. Patients suffer from rapid muscle atrophy, becoming debilitated and bedridden. Without proper use of language, they struggle to communicate properly, if at all.
No current drug is available to entirely halt the neurodegeneration caused by Alzheimer’s. However, the ability to predict the onset of the disease may aid in slowing down neurodegeneration.
While this study cannot save patients already in the terminal stages of Alzheimer’s, it provides hope to eradicate the emotional and physical implications of the disease in future generations.
