The Food and Drug Administration (FDA) approved on April 10th a brain imaging method for individuals who are being evaluated for Alzheimer's Disease (AD) or other causes of progressive cognitive impairment. The new method uses a drug called Amyvid (also known as Florbetapir or AV-45) along with Positron Emission Tomography (PET). MGH ADRC researchers were co-investigators for the clinical trial in which Amyvid was developed and have used this and other, similar PET methods for research purposes since 2005.
Two research studies, co-led by UC Davis neurologist Charles DeCarli and conducted by an international team that included more than 80 scientists at 71 institutions in eight countries, has advanced understanding of the genetic components of Alzheimer's disease and of brain development. Both studies appear in the April 15 edition of the journal Nature Genetics.
Worldwide, nearly 35.6 million people live with dementia. This number is expected to double by 2030 (65.7 million) and more than triple by 2050 (115.4 million). Dementia affects people in all countries, with more than half (58%) living in low- and middle-income countries. BY 2050, this is likely to rise to more than 70%.
Treating and caring for people with dementia currently costs the world more than US$604 billion per year. This includes the cost of providing health and social care as well as the reduction or loss of income of people with dementia and their caregivers.
The Food and Drug Administration (FDA) has approved Amyvid (florbetapir F18 injection), Avid Pharmaceuticals/Eli Lilly and Company's positron emission tomography (PET) tracer, for A-Beta plaque imaging in cognitively impaired patients being clinically evaluated for Alzheimer's disease. The compound will be available for use in June, with the aim of helping researchers rule out - not diagnose - the disease.
Under normal circumstances, the tau protein is a hard-working participant in memory and normal brain functioning. But as is becoming increasingly evident, in Alzheimer's disease and other neurodegenerative diseases, tau not only ceases to play a productive role in brain health, but actually undergoes a Jekyll-and-Hyde transformation to become a misshapen villain that destroys brain cells.
In Danville, California, the Traditions Alzheimer's Care Unit houses 20 residents, most of who are shepherded by caregivers through scheduled activities like balloon baseball and bingo. For most residents, life is routine.
But for Lee Gorewitz, life is an odyssey.
From the moment she wakes up, Lee is on a quest for something that she can neither articulate nor comprehend. Confined by the limits of her physical boundaries, she scavenges for reminders of her old identity in the outside world.
Our fond or fearful memories - that first kiss or a bump in the night - leave memory traces that we may conjure up in the remembrance of things past, complete with time, place and all the sensations of the experiences. Neuroscience call these traces memory engrams.
2012 Alzheimer's Disease Facts and Figures provides a statistical resource for U.S. data related to Alzheimer's dsiease, the most common type of dementia, as well as other dementias. Background and context for interpretation of the data are contained in the Overview. This information includes definitions of the types of dementia and a summary of current knowledge about Alzheimer's disease.
Two independent laboratories -- one at Columbia University; the other, at Harvard Medical School -- have devised a clever set of experiments to prove that the pathology that leads to tangle formation in Alzheimer disease (AD) spreads across the brain from neuron to neuron rather than selectively hitting vulnerable regions at different time points over the course of the disease.
The finding answers a pivotal question as to how AD progresses, and could open the door to novel treatments that could stop the disease from spreading and damaging key cognitive circuits.
Repression of certain gene activity in the brain appears to be an early event affecting people with Alzheimer's disease, a new study found. In mouse models of Alzheimer's disease, this blockage and its effet on memory were treatable.
Alzheimer's disease is the most common cause of dementia in older adults. It affects as many as 5.1 million Americans. A hallmark of the disease is the accumulation of a toxic protein fragment called beta-amyloid in brain nerve cells (neurons). Preventing the cognitive problems that result has been a major medical challenge.