Citations 2
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.
Consensus Recommendations to Accelerate Clinical Trials for Neurofibromatosis Type 2
Evans, D. Gareth , Kalamarides, Michel , Hunter‐Schaedle, Kim, Allen, Jeffrey C. , Babovic-Vuskanovic, Dusica, Belzberg, Allan J. , Bollag, Gideon , Chen, Ruihong , DiTomaso, Emmanuelle, Golfinos, John G. , Harris, Gordon J. , Jacob, Abraham, Kalpana, Ganjam V. , Karajannis, Matthias A. , Korf, Bruce R. , Law, Meng , McClatchey, Andrea I. , Packer, Roger J. , Roehm, Pamela C. , Rubenstein, Allan E., Slattery, William H. , Tonsgard, James H. , Widemann, Brigitte C. , Yohay, Kaleb , Giovannini, Marco , Blakeley, Jaishri O. , Kurzrock, Razelle , Welling, D. Bradley , Evans, D Gareth , Karajannis, Matthias A
Clinical Cancer Research | August 12, 2009 | Volume: 15 | Issue: 16 | Pages: 5032-5039
Abstract Purpose: Neurofibromatosis type 2 (NF2) is a rare autosomal dominant disorder associated primarily with bilateral schwannomas seen on the superior vestibular branches of the eighth cranial nerves. Significant morbidity can result from surgical treatment of these tumors. Meningiomas, ependymomas, and other benign central nervous system tumors are also common in NF2. The lack of effective treatments for NF2 marks an unmet medical need. Experimental Design: Here, we provide recommendations from a workshop, cochaired by Drs. D. Gareth Evans and Marco Giovannini, of 36 international researchers, physicians, representatives of the biotechnology industry, and patient advocates on how to accelerate progress toward NF2 clinical trials. Results: Workshop participants reached a consensus that, based on current knowledge, the time is right to plan and implement NF2 clinical trials. Obstacles impeding NF2 clinical trials and how to address them were discussed, as well as the candidate therapeutic pipeline for NF2. Conclusions: Both phase 0 and phase II NF2 trials are near-term options for NF2 clinical trials. The number of NF2 patients in the population remains limited, and successful recruitment will require ongoing collaboration efforts between NF2 clinics. (Clin Cancer Res 2009;15(16):5032–9)