List of publications for July 18, 2022
Effects of chronic cannabidiol in a mouse model of naturally occurring neuroinflammation, neurodegeneration, and spontaneous seizures
(2022) Scientific Reports, 12 (1), art. no. 11286, .
Dearborn, J.T.a , Nelvagal, H.R.b , Rensing, N.R.c , Takahashi, K.b , Hughes, S.M.d , Wishart, T.M.e , Cooper, J.D.b , Wong, M.c , Sands, M.S.a f
a Department of Medicine, Washington University School of Medicine, 4444 Forest Park Blvd Ave. 05536, St. Louis, MO 63110, United States
b Department of Pediatrics, Washington University School of Medicine, St. Louis, MO, United States
c Department of Neurology, Washington University School of Medicine, St. Louis, MO, United States
d Department of Biochemistry, University of Otago, Dunedin, New Zealand
e The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, United Kingdom
f Department of Genetics, Washington University School of Medicine, 4444 Forest Park Ave. 05509, St. Louis, MO 63110, United States
Abstract
Cannabidiol (CBD) has gained attention as a therapeutic agent and is purported to have immunomodulatory, neuroprotective, and anti-seizure effects. Here, we determined the effects of chronic CBD administration in a mouse model of CLN1 disease (Cln1−/−) that simultaneously exhibits neuroinflammation, neurodegeneration, and spontaneous seizures. Proteomic analysis showed that putative CBD receptors are expressed at similar levels in the brains of Cln1−/− mice compared to normal animals. Cln1−/− mice received an oral dose (100 mg/kg/day) of CBD for six months and were evaluated for changes in pathological markers of disease and seizures. Chronic cannabidiol administration was well-tolerated, high levels of CBD were detected in the brain, and markers of astrocytosis and microgliosis were reduced. However, CBD had no apparent effect on seizure frequency or neuron survival. These data are consistent with CBD having immunomodulatory effects. It is possible that a higher dose of CBD could also reduce neurodegeneration and seizure frequency. © 2022, The Author(s).
Funding details
Batten Disease Support and Research AssociationBDSRANIH NS R21 106523, NS R01100779, P50 HD103525
Biotechnology and Biological Sciences Research CouncilBBSRCBBS/E/D/10002071
Document Type: Article
Publication Stage: Final
Source: Scopus
Soft, bioresorbable coolers for reversible conduction block of peripheral nerves
(2022) Science, 377 (6601), pp. 109-115.
Reeder, J.T.a b c , Xie, Z.d e , Yang, Q.c f , Seo, M.-H.b c g , Yan, Y.h , Deng, Y.i , Jinkins, K.R.c , Krishnan, S.R.b c , Liu, C.c j , McKay, S.j , Patnaude, E.j , Johnson, A.j , Zhao, Z.d e , Kim, M.J.k , Xu, Y.l , Huang, I.b c , Avila, R.f , Felicelli, C.m , Ray, E.n , Guo, X.d e , Ray, W.Z.h n , Huang, Y.b c f o , MacEwan, M.R.h n , Rogers, J.A.b c f j p q r
a Knight Campus for Accelerating Scientific Impact, University of Oregon, Eugene, OR, United States
b Department of Materials Science and Engineering, Northwestern University, Evanston, IL, United States
c Querrey Simpson Institute for Bioelectronics, Northwestern University, Evanston, IL, United States
d State Key Laboratory of Structural Analysis for Industrial Equipment, Department of Engineering Mechanics, Dalian University of Technology, Dalian, China
e Ningbo Institute of Dalian University of Technology, Ningbo, China
f Department of Mechanical Engineering, Northwestern University, Evanston, IL, United States
g School of Biomedical Convergence Engineering, College of Information and Biomedical Engineering, Pusan National University, Busan, South Korea
h Department of Neurological Surgery, Washington University School of Medicine, St. Louis, MO, United States
i State Key Laboratory of Mechanical System and Vibration, Shanghai Jiao Tong University, Shanghai, China
j Department of Biomedical Engineering, Northwestern University, Evanston, IL, United States
k Department of Chemical Engineering, Northwestern University, Evanston, IL, United States
l Institute of Materials Science and Engineering, Washington University, St. Louis, MO, United States
m Department of Pathology, Northwestern University, Evanston, IL, United States
n Department of Biomedical Engineering, Washington University, St. Louis, MO, United States
o Departments of Civil and Environmental Engineering, Northwestern University, Evanston, IL, United States
p Department of Chemistry, Northwestern University, Evanston, IL, United States
q Department of Electrical Engineering and Computer Science, Northwestern University, Evanston, IL, United States
r Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Evanston, IL, United States
Abstract
Implantable devices capable of targeted and reversible blocking of peripheral nerve activity may provide alternatives to opioids for treating pain. Local cooling represents an attractive means for on-demand elimination of pain signals, but traditional technologies are limited by rigid, bulky form factors; imprecise cooling; and requirements for extraction surgeries. Here, we introduce soft, bioresorbable, microfluidic devices that enable delivery of focused, minimally invasive cooling power at arbitrary depths in living tissues with real-time temperature feedback control. Construction with water-soluble, biocompatible materials leads to dissolution and bioresorption as a mechanism to eliminate unnecessary device load and risk to the patient without additional surgeries. Multiweek in vivo trials demonstrate the ability to rapidly and precisely cool peripheral nerves to provide local, on-demand analgesia in rat models for neuropathic pain. © 2022 American Association for the Advancement of Science. All rights reserved.
Document Type: Article
Publication Stage: Final
Source: Scopus
A randomized feasibility study evaluating temozolomide circadian medicine in patients with glioma
(2022) Neuro-Oncology Practice, 9 (3), pp. 193-200. Cited 1 time.
Damato, A.R.a c , Katumba, R.G.N.d , Luo, J.a b , Atluri, H.d , Talcott, G.R.d , Govindan, A.d h , Slat, E.A.g , Weilbaecher, K.N.d , Tao, Y.a b , Huang, J.d , Butt, O.H.d , Ansstas, G.d , Johanns, T.M.d , Chheda, M.G.d , Herzog, E.D.c f , Rubin, J.B.e f , Campian, J.L.d
a Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St. Louis, MO, United States
b Siteman Cancer Center Biostatistics Core, Washington University School of Medicine, St. Louis, MO, United States
c Department of Biology, Washington University, St Louis, MO, United States
d Division of Oncology, Department of Medicine, Washington University School of Medicine, St Louis, MO, United States
e Department of Pediatrics, Washington University School of Medicine, St Louis, MO, United States
f Department of Neuroscience, Washington University School of Medicine, St Louis, MO, United States
g Department of Psychiatry, Washington University School of Medicine, St Louis, MO, United States
h John T. Milliken Department of Medicine, Washington University School of Medicine, St Louis, MO, United States
Abstract
Background: Gliomas are the most common primary brain tumor in adults. Current treatments involve surgery, radiation, and temozolomide (TMZ) chemotherapy; however, prognosis remains poor and new approaches are required. Circadian medicine aims to maximize treatment efficacy and/or minimize toxicity by timed delivery of medications in accordance with the daily rhythms of the patient. We published a retrospective study showing greater anti-tumor efficacy for the morning, relative to the evening, administration of TMZ in patients with glioblastoma. We conducted this prospective randomized trial to determine the feasibility, and potential clinical impact, of TMZ chronotherapy in patients with gliomas (NCT02781792). Methods: Adult patients with gliomas (WHO grade II-IV) were enrolled prior to initiation of monthly TMZ therapy and were randomized to receive TMZ either in the morning (AM) before 10 am or in the evening (PM) after 8 pm. Pill diaries were recorded to measure compliance and FACT-Br quality of life (QoL) surveys were completed throughout treatment. Study compliance, adverse events (AE), and overall survival were compared between the two arms. Results: A total of 35 evaluable patients, including 21 with GBM, were analyzed (18 AM patients and 17 PM patients). Compliance data demonstrated the feasibility of timed TMZ dosing. There were no significant differences in AEs, QoL, or survival between the arms. Conclusions: Chronotherapy with TMZ is feasible. A larger study is needed to validate the effect of chronotherapy on clinical efficacy. © 2022 The Author(s) 2022. Published by Oxford University Press on behalf of the Society for Neuro-Oncology and the European Association of Neuro-Oncology. All rights reserved.
Author Keywords
chronotherapy; feasibility; gliomas; quality of life
Document Type: Article
Publication Stage: Final
Source: Scopus
Identification of the Aβ37/42 peptide ratio in CSF as an improved Aβ biomarker for Alzheimer’s disease
(2022) Alzheimer’s and Dementia, .
Liu, L.a , Lauro, B.M.a , He, A.a , Lee, H.a , Bhattarai, S.b , Wolfe, M.S.b , Bennett, D.A.c , Karch, C.M.d e , Young-Pearse, T.a , Selkoe, D.J.a , Dominantly Inherited Alzheimer Network (DIAN)f
a Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, United States
b Department of Medicinal Chemistry, University of Kansas, Lawrence, KS, United States
c Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL, United States
d Department of Psychiatry, Washington University in St. Louis, St. Louis, MO, United States
e Hope Center for Neurologic Disorders, St. Louis, MO, United States
Abstract
Introduction: Identifying CSF-based biomarkers for the β-amyloidosis that initiates Alzheimer’s disease (AD) could provide inexpensive and dynamic tests to distinguish AD from normal aging and predict future cognitive decline. Methods: We developed immunoassays specifically detecting all C-terminal variants of secreted amyloid β-protein and identified a novel biomarker, the Aβ 37/42 ratio, that outperforms the canonical Aβ42/40 ratio as a means to evaluate the γ-secretase activity and brain Aβ accumulation. Results: We show that Aβ 37/42 can distinguish physiological and pathological status in (1) presenilin-1 mutant vs wild-type cultured cells, (2) AD vs control brain tissue, and (3) AD versus cognitively normal (CN) subjects in CSF, where 37/42 (AUC 0.9622) outperformed 42/40 (AUC 0.8651) in distinguishing CN from AD. Discussion: We conclude that the Aβ 37/42 ratio sensitively detects presenilin/γ-secretase dysfunction and better distinguishes CN from AD than Aβ42/40 in CSF. Measuring this novel ratio alongside promising phospho-tau analytes may provide highly discriminatory fluid biomarkers for AD. © 2022 the Alzheimer’s Association
Author Keywords
Alzheimer’s disease; amyloid β-protein; CSF biomarkers
Funding details
National Institutes of HealthNIHP30AG10161, PPG AG015379, R01 AG055909, R01 AG06173, R01 AG071865, R01AG15819, R01AG17917, R01AG30146, R01AG36836, R03AG063046, U01AG32984, U01AG46152
National Institute on AgingNIA
Alzheimer’s AssociationAA
Illinois Department of Public HealthIDPH
Fondation Brain Canada
Japan Agency for Medical Research and DevelopmentAMED
Translational Genomics Research InstituteTGEN
Canadian Institutes of Health ResearchIRSC
Fonds de Recherche du Québec – SantéFRQS
Korea Health Industry Development InstituteKHIDI
Instituto de Salud Carlos IIIISCIII
Deutsches Zentrum für Neurodegenerative ErkrankungenDZNE
Fleni
Document Type: Article
Publication Stage: Article in Press
Source: Scopus
Investing in Late-Life Brain Capital
(2022) Innovation in Aging, 6 (3), art. no. igac016, .
Dawson, W.D.a b c , Smith, E.b d , Booi, L.b e , Mosse, M.d , Lavretsky, H.f , Reynolds, C.F.g , Cummings, J.h , Brannally, P.i , Hynes, W.d , Lenze, E.J.j , Manes, F.k l , Ayadi, R.m , Frank, L.n , Chapman, S.B.o , Robertson, I.H.b o , Rubenstein, L.p , Jraissati, J.q , Ibáñez, A.b r , Fillit, H.s t , Jeste, D.V.u v , Rao, A.w x , Berk, M.y z , Storch, E.A.aa , Santuccione Chadha, A.ab ac , Eyre, H.A.y ad
a Department of Neurology, School of Medicine, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, CR131, Portland, OR 97239, United States
b Global Brain Health Institute at University of California, San Francisco (UCSF), San Francisco, CA, United States
c Trinity College Dublin, Dublin, Ireland
d Department of Medicine, Stanford Hospital, StanfordCA, United States
e Centre for Dementia Research, School of Health, Leeds Beckett University, Leeds, United Kingdom
f Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles (UCLA), Los Angeles, CA, United States
g Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, United States
h Chambers-Grundy Center for Transformative Neuroscience, Department of Brain Health, School of Integrated Health Sciences, University of Nevada, Las Vegas, NV, United States
i Alzheimer’s Disease Data Initiative, Gates Ventures, Redwood City, CA, United States
j Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, United States
k Institute of Cognitive and Translational Neuroscience (INCYT), INECO Foundation, Favaloro University, Buenos Aires, Argentina
l National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina
m Euro-Mediterranean Economists Association, Barcelona, Spain
n RAND Corporation, Arlington, VA, United States
o Center for BrainHealth®, University of Texas at Dallas, Dallas, TX, United States
p Australian Research Alliance for Children and Youth (ARACY), Canberra, ACT, Australia
q IESE Center for Public Leadership and Government, IESE Business School, Madrid, Spain
r Latin American Brain Health Institute (BrainLat), Universidad Adolfo Ibáñez, Santiago, Chile
s Alzheimer’s Drug Discovery Foundation (ADDF), New York City, NY, United States
t Departments of Geriatric Medicine, Palliative Care and Neuroscience, Icahn School of Medicine at Mount Sinai, New York City, NY, United States
u Departments of Psychiatry and Neurosciences, University of California San Diego, La JollaCA, United States
v IBM-UC San Diego Center for Artificial Intelligence for Healthy Living, University of California San Diego, La JollaCA, United States
w Neurocern, Chicago, IL, United States
x Department of Neurology, University of Toledo College of Medicine and Life Sciences, Toledo, OH, United States
y IMPACT, Institute for Mental and Physical Health and Clinical Translation, Deakin University, Geelong, VIC, Australia
z Department of Psychiatry, University of Melbourne, Melbourne, VIC, Australia
aa Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston, TX, United States
ab Biogen, Cambridge, MA, United States
ac Women’s Brain Project, Zurich, Switzerland
ad Neuroscience-inspired Policy Initiative, Organisation for Economic Co-operation and Development (OECD) and the PRODEO Institute, Paris, France
Abstract
Within many societies and cultures around the world, older adults are too often undervalued and underappreciated. This exacerbates many key challenges that older adults may face. It also undermines the many positive aspects of late life that are of tremendous value at both an individual and societal level. We propose a new approach to elevate health and well-being in late life by optimizing late-life Brain Capital. This form of capital prioritizes brain skills and brain health in a brain economy, which the challenges and opportunities of the 21st-century demands. This approach incorporates investing in late-life Brain Capital, developing initiatives focused on building late-life Brain Capital. © 2022 The Author(s) 2022.
Author Keywords
Aging; Brain health; Innovation; Mental disorders; Neuroscience; Psychiatry
Funding details
159418, GBHI ALZ UK-20-640170
BPIN2018000100059
National Institutes of HealthNIH
National Institute on AgingNIAP20AG068053, R01 AG057234, R01AG053798, R35AG71476
National Institute of General Medical SciencesNIGMSP20GM109025
National Institute of Neurological Disorders and StrokeNINDSU01NS093334
Alzheimer’s AssociationAASG-20-725707
Alzheimer’s Drug Discovery FoundationADDF
American Nurses FoundationANF
Eunice Kennedy Shriver National Institute of Child Health and Human DevelopmentNICHDP50HD103555
Rainwater Charitable FoundationRCF
National Health and Medical Research CouncilNHMRC1156072
Fondo Nacional de Desarrollo Científico y TecnológicoFONDECYT1210176, 1210195, ANID/FONDAP/15150012, FONCYT-PICT 2017-1820
Consejo Nacional de Investigaciones Científicas y TécnicasCONICET
Universidad del ValleUnivalleCI 5316, GBHI ALZ UK-20-639295
Document Type: Article
Publication Stage: Final
Source: Scopus
Pattern and degree of individual brain atrophy predicts dementia onset in dominantly inherited Alzheimer’s disease
(2021) Alzheimer’s and Dementia: Diagnosis, Assessment and Disease Monitoring, 13 (1), art. no. e12197, .
Keret, O.a , Staffaroni, A.M.b , Ringman, J.M.c , Cobigo, Y.b , Goh, S.-Y.M.b , Wolf, A.b , Allen, I.E.a d , Salloway, S.e , Chhatwal, J.f , Brickman, A.M.g , Reyes-Dumeyer, D.g , Bateman, R.J.h i j k l , Benzinger, T.L.S.h j , Morris, J.C.h i j k l , Ances, B.M.h i j k l , Joseph-Mathurin, N.h i j k l , Perrin, R.J.h i j k l , Gordon, B.A.h i j k l , Levin, J.m n , Vöglein, J.m n , Jucker, M.o p , la Fougère, C.o q , Martins, R.N.r s t u v , Sohrabi, H.R.r s t u v , Taddei, K.s u , Villemagne, V.L.w , Schofield, P.R.x y , Brooks, W.S.x z , Fulham, M.aa , Masters, C.L.ab , Ghetti, B.ac , Saykin, A.J.ad ae , Jack, C.R.af , Graff-Radford, N.R.ag , Weiner, M.ah ai aj ak al , Cash, D.M.am an , Allegri, R.F.ao , Chrem, P.ao , Yi, S.ap , Miller, B.L.a b , Rabinovici, G.D.a , Rosen, H.J.a b , Dominantly Inherited Alzheimer Networkaq
a Global Brain Health Institute, University of California, San Francisco, CA, United States
b Department of Neurology, Memory and Aging Center, University of California, San Francisco, CA, United States
c Alzheimer’s Disease Research Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States
d Department of Epidemiology and Biostatistics, University of California, San Francisco, CA, United States
e Warren Alpert Medical School, Brown University, Providence, RI, United States
f Massachusetts General Hospital, Harvard Medical School Boston, Boston, MA, United States
g Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University, New York, NY, United States
h Charles F. and Joanne Knight Alzheimer Disease Research Center, Department of Neurology, Washington University School of Medicine, St. Louis, MO, United States
i Department of Neurology, Washington University School of Medicine, St. Louis, MO, United States
j Department of Radiology, Washington University School of Medicine, St. Louis, MO, United States
k Division of Neuropathology, Department of Pathology & Immunology, Washington University School of Medicine, St. Louis, MO, United States
l Division of Biostatistics, Department of Psychiatry, Washington University in St. Louis School of Medicine, St. Louis, MO, United States
m German Center for Neurodegenerative Diseases (DZNE), Munich, Germany
n Department of Neurology, Ludwig-Maximilians-Universität München, Munich, Germany
o German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany
p Department of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany
q Institute for Nuclear Medicine and Clinical Molecular Imaging, Eberhard Karls University, Tübingen, Germany
r Department of Biomedical Sciences, Macquarie University, North Ryde, NSW, Australia
s Centre of Excellence for Alzheimer’s Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, WA, Australia
t School of Psychiatry and Clinical Neurosciences, University of Western Australia, Crawley, WA, Australia
u Australian Alzheimer’s Research Foundation, Nedlands, WA, Australia
v The Cooperative Research Centre for Mental Health, Carlton South, VIC, Australia
w Department of Molecular Imaging and Therapy, Austin Health, Melbourne, VIC, Australia
x Neuroscience Research Australia, Randwick, Sydney, NSW, Australia
y School of Medical Sciences, UNSW Sydney, Sydney, NSW, Australia
z Prince of Wales Hospital Clinical School, UNSW Sydney, Sydney, NSW, Australia
aa Department of Molecular Imaging, Royal Prince Alfred Hospital, Sydney Medical School, University of Sydney, Camperdown, NSW, Australia
ab The Florey Institute, University of Melbourne, Parkville, VIC, Australia
ac Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, United States
ad Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, United States
ae Department of Radiology, Indiana University School of Medicine, Indianapolis, IN, United States
af Department of Radiology, Mayo Clinic, Rochester, MN, United States
ag Department of Neurology, Mayo Clinic, Jacksonville, FL, United States
ah Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, San Francisco, CA, United States
ai Department of Radiology, University of California, San Francisco, San Francisco, CA, United States
aj Department of Medicine, University of California, San Francisco, San Francisco, CA, United States
ak Department of Psychiatry, University of California, San Francisco, San Francisco, CA, United States
al Department of Neurology, University of California, San Francisco, San Francisco, CA, United States
am Dementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, United Kingdom
an Centre for Medical Image Computing, Department of Medical Physics and Biomedical Engineering, University College London, London, United Kingdom
ao Department of Cognitive Neurology, Neuropsychiatry and Neuropsychology, Instituto de InvestigacionesNeurológicas FLENI, Buenos Aires, Argentina
ap Banner Alzheimer’s Institute, Phoenix, AZ, United States
Abstract
Introduction: Asymptomatic and mildly symptomatic dominantly inherited Alzheimer’s disease mutation carriers (DIAD-MC) are ideal candidates for preventative treatment trials aimed at delaying or preventing dementia onset. Brain atrophy is an early feature of DIAD-MC and could help predict risk for dementia during trial enrollment. Methods: We created a dementia risk score by entering standardized gray-matter volumes from 231 DIAD-MC into a logistic regression to classify participants with and without dementia. The score’s predictive utility was assessed using Cox models and receiver operating curves on a separate group of 65 DIAD-MC followed longitudinally. Results: Our risk score separated asymptomatic versus demented DIAD-MC with 96.4% (standard error = 0.02) and predicted conversion to dementia at next visit (hazard ratio = 1.32, 95% confidence interval [CI: 1.15, 1.49]) and within 2 years (area under the curve = 90.3%, 95% CI [82.3%–98.2%]) and improved prediction beyond established methods based on familial age of onset. Discussion: Individualized risk scores based on brain atrophy could be useful for establishing enrollment criteria and stratifying DIAD-MC participants for prevention trials. © 2021 The Authors. Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring published by Wiley Periodicals, LLC on behalf of Alzheimer’s Association
Author Keywords
autosomal dominant Alzheimer’s disease; brain atrophy; Dominantly Inherited Alzheimer Network; preclinical Alzheimer’s disease
Funding details
P01 AG003991, P01 AG026276
National Institutes of HealthNIHK08AG022228, K24 AG045333, P30 AG010133, P30 AG066444, P50AG005142, P50AG016570, R01 AG019771, R01 AG057739, R01 AG068193, R01 LM013463, U01 AG024904, U01 AG045390, U01 AG068057, U01AG051218, U19 AG032438, U19 AG063911, U54 NS092089
U.S. Department of DefenseDOD
National Institute on AgingNIA
U.S. Department of Veterans AffairsVA
Mayo Clinic
Alzheimer’s AssociationAAAARFD‐20‐681815, UF1AG032438
Larry L. Hillblom FoundationLLHF
Eli Lilly and Company
Roche
California Department of Public HealthCDPH
Patient-Centered Outcomes Research InstitutePCORI
Alzheimer’s Disease Research Center, Emory UniversityADRCP01 AG019724, P30 AG062422, R01 AG057234, T32 AG023481
Japan Agency for Medical Research and DevelopmentAMED
Stroke FoundationSF
Buck Institute for Research on Aging
Avid Radiopharmaceuticals
Rainwater Charitable FoundationRCF
Australian Catholic UniversityACU
Korea Health Industry Development InstituteKHIDI
Deutsches Zentrum für Neurodegenerative ErkrankungenDZNE
Fleni
NIHR Cambridge Biomedical Research Centre
Document Type: Article
Publication Stage: Final
Source: Scopus