As the world's population continues to age, Alzheimer's disease presents a looming public health crisis that, left unchecked, threatens to overwhelm health care systems throughout the developed world. In order to significantly tackle the most catastrophic and devastating symptom of Alzheimer's disease (AD)--dementia--we must be able to detect the disease prior to the onset of clinical symptoms, and be able to offer patients preventative treatments that block or significantly slow disease progression. This review summarizes a variety of the most promising early detection methods for Alzheimer's disease (AD) and mild cognitive impairment (MCI) that could be used to identify those at high risk of developing the disease and used for monitoring disease progression and response to investigational treatments. In addition, treatment research programs that could be developed into disease-modifying treatments that significantly delay the development of dementia are highlighted. These potential treatments target many different pathways, and may one day be dosed in combination to increase efficacy and prevent cognitive deterioration in patients with AD. While we still face numerous challenges, AD researchers have made great progress in understanding disease mechanisms. As we have seen in the treatment of heart disease, even modest preventative treatments can have hugely significant clinical outcomes and drastically reduce disease prevalence on a population scale. Therefore, there is hope that the development of prophylactic treatments, combined with improved early detection methods, will provide dramatic relief for millions of aging individuals threatened by the specter of Alzheimer's disease.
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http://dx.doi.org/10.31887/DCNS.2009.11.2/dwshineman | DOI Listing |
Alzheimers Dement
January 2025
Virginia Center on Aging, College of Health Professions, Virginia Commonwealth University, Richmond, Virginia, USA.
Introduction: The Virginia Memory Project (VMP) is a statewide epidemiological registry for Alzheimer's disease and related disorders (ADRD) and other neurodegenerative conditions. It aims to support dementia research, policy, and care by leveraging the Centers for Disease Control (CDC) Healthy Brain Initiative (HBI) Roadmap.
Methods: To capture comprehensive data, the VMP integrates self-enrollment and automatic enrollment using Virginia's All-Payer Claims Database (APCD).
Brain
January 2025
Comprehensive Epilepsy Program, Department of Neurology, University of Virginia, Charlottesville, Virginia 22908, USA.
Seizures in people with dementia (PWD) are associated with faster cognitive decline and worse clinical outcomes. However, the relationship between ongoing seizure activity and postmortem neuropathology in PWD remains unexplored. We compared post-mortem findings in PWD with active, remote, and no seizures using multicentre data from 39 Alzheimer's Disease Centres from 2005 to 2021.
View Article and Find Full Text PDFBrain
January 2025
Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, 22184 Lund, Sweden.
The APOE4 allele is the strongest genetic risk factor for sporadic Alzheimer's disease (AD). While APOE4 is strongly associated with amyloid-beta (Aβ), its relationship with tau accumulation is less understood. Studies evaluating the role of APOE4 on tau accumulation showed conflicting results, particularly regarding the independence of these associations from Aβ load.
View Article and Find Full Text PDFJ Int Neuropsychol Soc
January 2025
Department of Brain Health, University of Nevada, Las Vegas, NV, USA.
Objective: Neuropsychiatric symptoms (NPS) are considered diagnostic and prognostic indicators of dementia and are attributable to neurodegenerative processes. Little is known about the prognostic value of early NPS on executive functioning (EF) decline in Alzheimer's disease and related dementias (ADRD). We examined whether baseline NPS predicted the rate of executive function (EF) decline among older adults with ADRD.
View Article and Find Full Text PDFIntroduction: Age-associated depletion in nicotinamide adenine dinucleotide (NAD+) concentrations has been implicated in metabolic, cardiovascular, and neurodegenerative disorders. Supplementation with NAD+ precursors, such as nicotinamide riboside (NR), offers a potential therapeutic avenue against neurodegenerative pathologies in aging, Alzheimer's disease, and related dementias. A crossover, double-blind, randomized placebo (PBO) controlled trial was conducted to test the safety and efficacy of 8 weeks' active treatment with NR (1 g/day) on cognition and plasma AD biomarkers in older adults with subjective cognitive decline and mild cognitive impairment.
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