RESEARCH NEWS 2014-09-16 Research News Valium can make people pleasantly foggy, which is a reason doctors prescribe it to relieve stress during outpatient surgeries and for anxiety and panic attacks. However, a new study suggests that the effects of prolonged use of benzodiazepin
CONFERENCE COVERAGE 2006-11-05 Conference Coverage This past August, Alzheimer disease researchers met with colleagues from other fields and with foundation and NIH representatives in Bar Harbor, Maine, at the sixth annual workshop on Enabling Technologies for Alzheimer Disease Researc
CONFERENCE COVERAGE 2006-11-05 Conference Coverage To what extent is AD an acceleration of normal aging? This decades-old question receded in favor of the view that AD is a separate process from normal aging when studies showed that patterns of neuronal loss are different in aging and
CONFERENCE COVERAGE 2006-11-05 Conference Coverage Genomic/proteomic/metabolomics (OMICS) research in AD remains in its infancy. Most studies stall after discovering lists of hundreds of genes whose expression changes in the chosen comparison. Few groups have been able to validate thei
CONFERENCE COVERAGE 2006-11-05 Conference Coverage I. Immune mechanisms in aging and Alzheimer disease Determine whether endogenous immune mechanisms in the brain can be modulated to alter brain function or disease processes. Study differences between immune modulation in mice and huma
RESEARCH NEWS 2014-09-18 Research News Some people seem to cope better than others with having amyloid plaques in their brains. According to a study in the September 14 Nature Neuroscience, they maintain cognitive prowess by kicking neural networks into overdrive. Such hyperactiv
RESEARCH NEWS 2014-09-18 Research News With predictions of a coming global avalanche of dementia cases, researchers are turning their attention to prevention strategies. Based on current data, at least four lifestyle factors robustly affect dementia risk, according to the World A
CONFERENCE COVERAGE 2005-09-10 Conference Coverage In August 2005, a group of researchers from inside and outside the field of Alzheimer disease met in Bar Harbor, Maine, with foundation and NIH representatives for two days of presentations and discussion at the fifth annual workshop o
CONFERENCE COVERAGE 2005-09-10 Conference Coverage It is widely accepted that at least a fraction of APP is actively transported along the axon to the nerve terminal and does not return to the cell body. Current points of debate on APP and axonal transport include whether APP binds dir
CONFERENCE COVERAGE 2005-09-10 Conference Coverage After release, some Aβ is degraded locally, a second fraction leaves the brain through interstitial fluid drainage and along brain arterioles, while another fraction is actively transported by proteins, such as LRP and glycoprotein-P,
CONFERENCE COVERAGE 2005-09-10 Conference Coverage Clearly, the greatest risk factor for AD is advanced age, but a satisfying explanation of the link between aging and AD remains uncertain. To understand this connection, it is argued that a better understanding of "normal" ag
CONFERENCE COVERAGE 2005-09-10 Conference Coverage This workshop has an enduring interest in facilitating the import into AD research of new technologies developed in other areas. This year an approach was presented that makes it possible to watch neurons grow and change over time insi
CONFERENCE COVERAGE 2005-09-10 Conference Coverage I. Address gaps in our knowledge of APP processing, movement, and signaling. A. Questions to be addressed include: 1. Where in a neuron is Aβ made? This is an old question that should be settled. 2. Why is APP processed? What is the ph
CONFERENCE COVERAGE 2004-12-05 Conference Coverage This report summarizes discussions and recommendations made at the fourth annual workshop on Enabling Technologies for Alzheimer's disease (AD), held in August 2004 in Bar Harbor, Maine. Academic and industry scientists from insid
CONFERENCE COVERAGE 2004-12-05 Conference Coverage Axonal Transport Larry Goldstein, of University of California, San Diego, laid out his hypothesis that defects in axonal transport could starve the nerve terminal of needed supplies and lead to synaptic dysfunction in AD, Huntington