Alzheimer's disease progressively kills brain cells, deleting memories, muddling analytical thinking, altering personality and ultimately limiting mobility. As the most common form of dementia in people over the age of 65, according to the National Institute of Neurological Disorders and Stroke, better diagnosis and treatment for patients with Alzheimer's remain a high priority.
Genetics
Scientists know that genetic factors contribute to a person's likelihood of developing Alzheimer's disease, but they have not identified all of the genes that play a role in determining risk. A July 2010 press release from the Alzheimer's Association summarizes research identifying a new gene, called FTO, that increases the risk for Alzheimer's disease. The FTO gene, known to be involved in obesity, contributes to Alzheimer's even after its effects on cardiovascular health--an independent risk factor--are removed from analysis. Researchers found that the AA form of FTO increased the risk of Alzheimer's disease by 58 percent compared to people with the TT variant. In addition, FTO apparently interacts with another Alzheimer's gene called the APOE gene. People with the AA variant of FTO and the high risk APOEε4 variant had double the risk of developing Alzheimer's disease.
Diagnosis
Early diagnosis of Alzheimer's disease can allow patients to begin therapy before too much damage has been done. In the June 30, 2010, issue of "Neurology," Dr. Susan Landau and her colleagues reported that a type of PET imaging called FDG-PET can help predict who will develop Alzheimer's disease. In this study, patients with mild memory problems who scored poorly on a memory test and had abnormal results with FDG-PET had almost 12 times the risk of developing Alzheimer's disease within the next year and a half or so, compared to people with normal results on both tests. FDG-PET could also predict the rate of decline in Alzheimer's, although the ratio of an abnormal tau protein to beta amyloid in spinal fluid was a better marker.
Immunotherapies
Alzheimer's disease causes the accumulation of abnormal protein deposits called plaques and tangles in the brain, ultimately killing brain cells. Plaques form from deposits of a protein called beta amyloid, while tangles consist of an abnormal version of the protein tau. Many scientists believed that ridding the brain of beta amyloid could cure or slow the progression of Alzheimer's disease, but evidence gathered in a July 2010 press release by the Alzheimer's Association suggests that tau might be a better target for therapy. Separate studies using rodents and humans showed that antibodies to tau or to beta amyloid decreased the amount of tau tangles. In the rodent studies, the immunotherapy treatments that reduced tau also improved measures of learning or memory.
References
- National Institute of Neurological Disorders and Stroke: Alzheimer's Disease
- Alzheimer's Association: Obesity Gene and Alzheimer's Disease
- "Neurology"; Comparing Predictors of Conversion and Decline in Mild Cognitive Impairment; S.M. Landau et al.; June 30, 2010.
- Alzheimer's Association: Experimental Immunotherapies for Alzheimer's
