Dr. Eric Reiman shares how brain imaging is used to evaluate cognitive impairment and Alzheimer's disease.
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Brain Imaging to Evaluate Cognitive Impairment and Alzheimer's disease There are now an increasing number of treatments that are intended to target the molecular vents that lead to those microscopic abnormalities. We see that in the brain at the end of life in patients that is amyloid plaques, neurofibril iori tangles and a loss of brain cells. The largest groups of treatments are this so called amyloid modified medication treatments. Passive immunization therapies and active immunization therapies to interfere with the accumulation of a protein called amyloid, which is the main component of those plaques I just described. If as many but not all researchers believe that amyloid plays a critical early role in the development of Alzheimer’s disease and its not just the consequence of the disease. If this treatments are sufficiently safe and well tolerated, if they’re targeting the right form of amyloid and if we intervene soon enough they maybe able to strike Alzheimer’s at its heart. There are smaller number of treatment that the chest beginning to be developed to target those tangles in the brain. Those tangles are main constituent of which is a protein called Tau, at least how modifying treatments we look forward to seeing more of them on the horizon being used by themselves or in combination of this amyloid modifying treatments. Further more there are other treatments that are designed to protect brain cells from the damaging effects of amyloid, tau or other toxic events that are being studied. Well I’m most excited at the moment about this amyloid modifying treatments. Even so there are many researchers who believe that this amyloid modifying treatments may have a more modest effect in clinically effective patients because the brain pathology is already fairly severed by them. Even if they fail to have the most profound effect in clinically effective patients and we sincerely hope that they have a profound effect. That would not be the death of the amyloid hypothesis. What it would compel us to do is to start thinking about intervening with those same treatments before the onset of symptoms, so what we need now is to know from those clinical trials and patients whether those treatments are sufficiently safe and well tolerated to try conducting prevention studies in healthy people. Starting with those healthy people with highest risks for Alzheimer’s disease so the risk versus benefits can be addressed. On given the devastating effect that Alzheimer’s disease takes on patients and families and the sky rocketing numbers of patients will be afflicted as more of us live to older ages. There's an urgent need to find treatment not just to stop Alzheimer’s in its tracks in affected patients but to prevent it. furthermore its been suggested that some of the promising treatments that are now being investigated in clinical trials in patients may have a more profound benefit if started before the onset of symptoms when we have less severe brain pathology. So there are numbers of investigational treatments were excited about for prevention and in addition there are number of other already available medications, dietary supplements and other healthy lifestyle interventions that just might have the possibility of reducing a persons risk of Alzheimer’s disease. Unfortunately we don’t know for sure which of these treatments are effective because right now would take too many healthy people on a clinical trial. Too many years, one with the life of a drug companies patent and too much money to wait in a clinical trial to see if those people receiving this sugar pill to have enough people who develop Alzheimer’s disease to see if the treatments work. We need new techniques to evaluate the ability to slow down the brain changes without having to wait to see if somebody will go on to develop symptoms. So we have been developing a strategy in which we’ve been using brain imaging techniques and other biologic markers of the disease.
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