2008 Alzheimer’s disease facts and figures

  title={2008 Alzheimer’s disease facts and figures},
  author={Alzheimer’s Association},
  journal={Alzheimer's \& Dementia},
Adult Day Health Care for Participants With Alzheimer’s Disease
Results demonstrate that ADHC providers are adapting to the cognitive and physical abilities of their participants; however, there is need for enhancing stage-specific services, especially for participants at later stages and for early-onset dementia.
Pathology of Neurodegenerative Diseases
As the average life expectancy has been extended by the current state-of-art medical technologies, the elderly population is increasing rapidly. The world is now facing the ‘ageing era’, which comes
Traumatic Brain Injury: Risk Factors and Biomarkers of Alzheimer's Disease and Chronic Traumatic Encephalopathy
  • R. Rubenstein
  • Biology, Medicine
    Current Translational Geriatrics and Experimental Gerontology Reports
  • 2012
In almost all of the studies investigating traumatic brain injury and AD risk, AD was diagnosed based on clinical criteria for probable or possible AD, without neuropathological verification, suggesting that the increased incidence of dementia following head injuries is due to CTE, alone or in conjunction with other neurodegenerative conditions such as AD.
Cardiometabolic Modification of Amyloid Beta in Alzheimer’s Disease Pathology
The contributions of individual cardiometabolic diseases including cardiovascular disease (CVD), type 2 diabetes (T2D), obesity, and non-alcoholic fatty liver disease (NAFLD) in elevating concentrations of circulating Aβ within the brain are highlighted, as well as the comorbid association of Aβ with AD pathology is discussed.
Mild cognitive impairment associates with concurrent decreases in serum cholesterol and cholesterol-related lipoprotein subclasses
Findings suggest that a decreasing trend in serum cholesterol measures in elderly individuals may suffice as an indication for more detailed inspection for potential signs of cognitive decline.
C-terminal peptides coassemble into Aβ42 oligomers and protect neurons against Aβ42-induced neurotoxicity
Aβ(31–42) and Aβ(39-42) are leads for obtaining mechanism-based drugs for treatment of AD using a systematic structure–activity approach.
Quantitative Pharmacology Approach in Alzheimer’s Disease: Efficacy Modeling of Early Clinical Data to Predict Clinical Outcome of Tesofensine
Effective therapeutic options for Alzheimer’s disease (AD) are limited and much research is currently ongoing. The high attrition rate in drug development is a critical issue. Here, the quantitative
Soluble aggregates of the amyloid-β peptide are trapped by serum albumin to enhance amyloid-β activation of endothelial cells
These results demonstrate that inhibitors of Aβ self-assembly have the potential to trap small soluble aggregates resulting in an elevation rather than a reduction of cellular responses, and provide further support that small soluble aggregation possess high levels of physiological activity.