Two recent releases on modest progress in Alzheimer's research are illustrative of the way in which this scientific community is driving the establishment of new biotechnology toolkits and a deep knowledge of brain biochemistry as a part of seeking a cure. Each new incremental advance adds a new piece to the biochemical puzzle and tool to the toolkit, there to be used in all research into the aging brain.
And, yes, we need all the research we can get - if we want to live far longer, healthier lives, we had better become very, very good at understanding and repairing the aging brain.
Scientists are in the early stages of identifying biomarkers in the blood and spinal fluid to help with Alzheimer's diagnosis, but this new study is the first to report a real time "window into the brain" that identifies both of the major abnormal deposits of the disease in living people who may not develop Alzheimer's for years to come.
Researchers performed PET brain scans after intravenously injecting the volunteers with the new chemical marker called FDDNP, the molecule that binds to the plaque and tangle deposits found in Alzheimer's disease.
Scientists found distinct differences among people with normal brain aging, patients with Alzheimer's disease and people with mild cognitive impairment.
The PET imaging showed that the more advanced the disease the higher the FDDNP concentration in areas where the abnormal protein deposits typically accumulate -- in the temporal, parietal and frontal brain regions. Patients with Alzheimer's disease showed the most FDDNP binding, indicating a higher level of plaques and tangles than other subjects.
"This is the first time this pattern of plaque and tangle accumulation has been tracked in living humans over time in a longitudinal study"
In a new animal study, the NYU School of Medicine researchers report that they have reduced by around 50 percent the aggregation of toxic amyloid protein in the brains of mice by blocking the interaction between a protein called apolipoprotein E (apo E) and amyloid. Apo E acts as a sort of biological chaperone, ferrying cholesterol and fats around the brain.
The researchers [created] a nontoxic, synthetic protein fragment or peptide that binds to apo E, preventing it from latching onto amyloid.
In a series of studies in transgenic mice, the peptide reduced the amount of plaque in the brain and the amount of amyloid in the brain's blood vessels. It did not cause any apparent inflammation or leaks in blood vessels in the animals' brains, according to the study. Finally, in another set of experiments, the treated mice did not exhibit any memory decline when they were put into a radial arm maze, which evaluates working memory based on the animals' behavior.
Even imperfect or partially effective therapies (or changes in lifestyle in many cases) can be of great benefit for age-related conditions if applied early on, in the very first stages - but to do that, you must have the ability to diagnose early. This ability has been greatly lacking for Alzheimer's patients until very recently, but none of the diagnostic work in progress is yet beyond trials and in widespread use:
The regulatory hurdles chew up years between laboratory and clinical practice these days - which is not to mention the many therapies and tests that are simply never developed because the regulatory costs are too high.