Moving beyond cell culture, neuroscientists are using CRISPR to tweak genes in living animals and perhaps, one day, as therapy in humans.
Researchers in the United States, France, and Austria honored for pioneering work on deep-brain stimulation and L-dopa.
When strict quality control standards are followed, low Aβ in cerebrospinal fluid accurately predicts amyloid plaques in people with cognitive impairment in clinical practice.
Expansions in ataxin 2 predispose people to the ALS end of the ALS-FTD spectrum, and never cause pure FTD, according to a new French study.
Prescribed to treat anxiety and insomnia, benzodiazepines may do more than put the mind at ease. A new study links their prolonged use to increased Alzheimer’s risk.
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 Research.
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 AD.
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.
Recommendations for future research from the Enabling Technologies for Alzheimer's Disease Research in Bar Harbor (2006).
Alzheimer Disease, Aging, and the Immune System Synaptic Function in Aging and AD High-throughput Assays (Application of OMICS to AD) Recommendations for Future Research Enabling Technologies for Alzheimer Disease Research: 2006 Bar Harbor Workshop ...
Overzealous neural responses may protect some amyloid-bearers from slipping into cognitive decline, a study suggests.
Controlling diabetes and hypertension and stopping smoking can slash dementia risk.
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 on Enabling Technologies for Alzheimer's Disease Research.
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.
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, across the blood-brain barrier (BBB) into systemic circulation.