Recently, scientists claimed to be succeeded in the hunt for biomarkers for Alzheimer's disease.
A biomarker is something that can be measured; it is an indicator of what is going on inside the body. Biomarker will assist in early detection, in testing new therapies and, once doctors have better drugs for Alzheimer's, with earlier intervention in the disease process.
Dr. Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City explained that if we are going to have any kind of medication that alters or modifies the disease, if it is really going to change it rather than treat symptoms, then we need biomarkers that are sensitive to the illness before a person becomes impaired. According to Kennedy, in Alzheimer's, we need two things: We need to figure out who's sick and who's not and, secondly, biomarkers should be treatment-sensitive, meaning if patients have got the right treatment, we can watch the biomarker go down, like blood sugar and insulin.
A study has found that differences in levels of CD-69, which is a protein involved in white blood cell production and growth. The study was being presented at the International Conference on Alzheimer's Disease (ICAD) in Chicago. Moreover, the study has allowed researchers to distinguish between people with Alzheimer's, people with Parkinson's-related dementia and those who were cognitively normal.
The researchers at the University of Leipzig in Germany were made the study based on a theory that Alzheimer's occurs when neurons get a false signal to divide. The more popular theory holds that a build-up of amyloid plaque (made up mostly of beta amyloid protein) in the brain causes Alzheimer's.
On the other hand, Kennedy said that the alternative theory about Alzheimer's is that the cells replication process gets triggered pathologically, and then the cells are programmed to die, and that is what is killing the nerve cells, not the amyloid. However, researchers still have a long way to go. It is one thing to distinguish the sick group from the healthy group and another to see if we can predict from the healthy group who gets the disease.
A second study, from researchers at Washington University in St. Louis, confirmed previous findings: that the more amyloid there is in the brain (as measured by PET scans), the less beta amyloid 42 there is in cerebrospinal fluid. Beta amyloid 42 is an extra-"sticky" type of amyloid protein that accumulates and forms plaques. The theory is that measurements of beta amyloid 42 in spinal fluid could serve as a marker for Alzheimer's disease.
On the other hand, another study found that individuals with mild cognitive impairment (MCI), often considered a transitional stage between normal cognitive functioning and Alzheimer's, had elevated levels of beta-secretase (BACE1) activity in the brain when compared to both healthy people and people with Alzheimer's. The study was made by a team in Ireland and in Germany
Finally yet importantly, a fourth study showed that a certain radioactive compound or tracer, 18F-AV-45, may have potential in the diagnosis and early detection of Alzheimer's when used with PET scans. Trials of the substance, conducted by Philadelphia-based Avid Radiopharmaceuticals Inc., are ongoing.
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