在早期阿尔茨海默氏症患者中进行了两项Gantenerumab第三期试验

Randall J Bateman1, Janice Smith1, Michael C Donohue1

  • 1From the Department of Neurology, Washington University School of Medicine, St. Louis (R.J.B.); Roche Products, Welwyn Garden City (J.S., C.L.), and the Department of Brain Sciences, Faculty of Medicine, Imperial College London (R.J.P.), and the Dementia Research Centre, Department of Neurodegenerative Disease, and the U.K. Dementia Research Institute, Queen Square Institute of Neurology, University College London (N.C.F.), London - all in the United Kingdom; the Alzheimer's Therapeutic Research Institute, Keck School of Medicine, University of Southern California, San Diego (M.C.D.), and Genentech, South San Francisco (T.B., R.S.D.) - both in California; F. Hoffmann-La Roche, Basel, Switzerland (P.D., R.A., J.W., T.B., G.K., A. Thanasopoulou, M. Baudler, P.F., R.S.D.); Butler Hospital and Warren Alpert Medical School, Brown University, Providence, RI (S.S.); the Department of Psychiatry and Neurochemistry, Sahlgrenska Academy, University of Gothenburg, and the Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital - both in Mölndal, Sweden (K.B.); the Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, and the L.C. Campbell Cognitive Neurology Research Unit, Dr. Sandra Black Centre for Brain Resilience and Recovery, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto - both in Toronto (S.E.B.); the Ace Alzheimer Center Barcelona, Universitat Internacional de Catalunya, Barcelona, and the Networking Research Center on Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, Madrid - both in Spain (M. Boada); the Department of Psychiatry and Psychotherapy, Klinikum rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany (T.G.); the Department of Neurology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan (A. Tamaoka); the Department of Neurology, Georgetown University School of Medicine, Washington, DC (R.S.T.); the Alzheimer's Research and Treatment Center, Wellington, FL (D.W.); the Medical and Cognitive Research Unit, Heidelberg Repatriation Hospital, Austin Health, Melbourne, VIC, Australia (M.W.); and the Chambers-Grundy Center for Transformative Neuroscience, Department of Brain Health, School of Integrated Health Sciences, University of Nevada, Las Vegas, Las Vegas (J.L.C.).

PubMed
概括

在阿尔茨海默氏症早期,甘鲁马布减少了粉样质斑块,但并没有减缓认知能力的下降. 这种单克隆抗体向beta-粉样蛋白,显示斑块减少,但在试验中没有显著的临床益处.

相关概念视频

Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
197
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
498
Parkinson's Disease: Treatment01:24

Parkinson's Disease: Treatment

Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...
281