Citations 2
A Workshop on Cognitive Aging and Impairment in the 9/11-Exposed Population
Daniels, Robert D. , Clouston, Sean , Hall, Charles B. , Anderson, Kristi , Bennett, David A. , Bromet, Evelyn J. , Calvert, Geoffrey M. , Carreón, Tania , Diminich, Erica D. , Kreisl, William Charles, Kritikos, Minos , Kubale, Travis L. , Mielke, Michelle M. , Peskind, Elaine R. , Raskind, Murray A. , Richards, Marcus , Sano, Mary , Santiago‐Colón, Albeliz , Sloan, Richard P. , Spiro, Avron , Vasdev, Neil , Reissman, Dori B. , Clouston, Sean A P , Anderson, Kristi R , Kritikos, Minos , Mielke, Michelle M , Santiago-Colón, Albeliz , Spiro, Avron , Vasdev, Neil , Bennett, David A. , DeKosky, Steven T. , Finch, Caleb E. , Gandy, Sam , Luft, Benjamin J.
International Journal of Environmental Research and Public Health | January 14, 2021 | Volume: 18 | Issue: 2 | Pages: 681
The terrorist attacks on 11 September 2001 potentially exposed more than 400,000 responders, workers, and residents to psychological and physical stressors, and numerous hazardous pollutants. In 2011, the World Trade Center Health Program (WTCHP) was mandated to monitor and treat persons with 9/11-related adverse health conditions and conduct research on physical and mental health conditions related to the attacks. Emerging evidence suggests that persons exposed to 9/11 may be at increased risk of developing mild cognitive impairment. To investigate further, the WTCHP convened a scientific workshop that examined the natural history of cognitive aging and impairment, biomarkers in the pathway of neurodegenerative diseases, the neuropathological changes associated with hazardous exposures, and the evidence of cognitive decline and impairment in the 9/11-exposed population. Invited participants included scientists actively involved in health-effects research of 9/11-exposed persons and other at-risk populations. Attendees shared relevant research results from their respective programs and discussed several options for enhancements to research and surveillance activities, including the development of a multi-institutional collaborative research network. The goal of this report is to outline the meeting’s agenda and provide an overview of the presentation materials and group discussion.
Vascular dysfunction—The disregarded partner of Alzheimer's disease
Sweeney, Melanie D. , Montagne, Axel , Nation, Daniel A. , Schneider, Lon S. , Chui, Helena C., Harrington, Michael G. , Pa, Judy , Law, Meng , Wang, Danny J.J. , Jacobs, Russell E. , Doubal, Fergus , Ramirez, Joel , Dichgans, Martin , Love, Seth , Bath, Philip M. , Markus, Hugh S. , Salman, Rustam Al‐Shahi , Kalaria, Rajesh N., Werring, David J. , Moskowitz, Michael A., Katušić, Zvonimir S. , Lazarov, Orly , Rehman, Jalees , Wellington, Cheryl L. , González, Héctor M. , Yuan, Chun , Lockhart, Samuel N. , Hughes, Timothy M. , Chen, Christopher , Sachdev, Perminder S. , O’Brien, John T. , Pantoni, Leonardo , Gustafson, Deborah , Biessels, Geert Jan , Wallin, Anders , Wong, Adrian , Passmore, Peter , Barkof, Frederick, Muller, Majon , Román, Gustavo C. , Hamel, Édith , Seshadri, Sudha , Buchem, Mark A. van , Arvanitakis, Zoe , Drewes, Lester R. , Hachinski, Vladimir , Wardlaw, Joanna M. , Kalaria, Raj N. , Dichgans, Martin , O'Brien, John Tiernan , Wardlaw, Joanna Marguerite , Seshadri, Sudha , Sachdev, Perminder S , Sagare, Abhay P. , Chui, Helena C. , Black, Sandra E. , Nedergaard, Maiken , Benveniste, Helene , Iadecola, Costantino , Allan, Stuart McRae , Quinn, Terence J , Carare, Roxana Octavia , Touyz, Rhian M. , Williams, Steven , Lutz, Sarah E. , Minshall, Richard D. , Davis, Thomas P. , Gonzalez, Hector M , Skoog, Ingmar , Biessels, Geert Jan , Smith, Eric Edward , Mok, Vincent , Breteler, Monique M.B. , Gottesman, Rebecca F. , Schneider, Julie A. , Finch, Caleb E. , Toga, Arthur W. , Zloković, Berislav V. , Al-Shahi Salman, Rustam , Werring, David John , Wang, Danny J J
Alzheimer's & Dementia | January 11, 2019 | Volume: 15 | Issue: 1 | Pages: 158-167
Abstract Increasing evidence recognizes Alzheimer's disease (AD) as a multifactorial and heterogeneous disease with multiple contributors to its pathophysiology, including vascular dysfunction. The recently updated AD Research Framework put forth by the National Institute on Aging–Alzheimer's Association describes a biomarker‐based pathologic definition of AD focused on amyloid, tau, and neuronal injury. In response to this article, here we first discussed evidence that vascular dysfunction is an important early event in AD pathophysiology. Next, we examined various imaging sequences that could be easily implemented to evaluate different types of vascular dysfunction associated with, and/or contributing to, AD pathophysiology, including changes in blood‐brain barrier integrity and cerebral blood flow. Vascular imaging biomarkers of small vessel disease of the brain, which is responsible for >50% of dementia worldwide, including AD, are already established, well characterized, and easy to recognize. We suggest that these vascular biomarkers should be incorporated into the AD Research Framework to gain a better understanding of AD pathophysiology and aid in treatment efforts.