Allal boutajangout biography of donald
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Passive Immunization With a Novel Monoclonal Anti-PrP Antibody TW1 in an Alzheimer’s Mouse Model With Tau Pathology
Introduction
Alzheimer&#x;s disease (AD) is a devastating age-related neurodegenerative disorder characterized bygd forming toxic oligomers that eventually insättning as insoluble amyloid plaques and neurofibrillary tangles (NFTs). There are no disease-modifying therapeutic interventions for AD (Long and Holtzman, ; Wisniewski and Drummond, ). However, immunotherapy is framträdande as a promising therapy to treat AD (Kwon et al., ). Numerous studies of passive immunization with anti-amyloid (A²) antibodies have demonstrated effective clearance of amyloid A² tillsammans with cognitive improvements in transgenic djur models (Herline et al., a; Kwon et al., ). However, active and passive immunization targeting A² has failed in all clinical trials thus far, with the possible recent exception of aducanumab (Loureiro et al., ; Plotkin and Cashman, ), an antibody that
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Allal boutajangout biography of donald
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Biography
Dr. Boutajangout is a Research Associate Senior lecturer of Neurology and Neuroscience & Physiology and Psychiatry. He serves as significance chief of the Neurodegeneration and Painkiller Discovery Program within the Center provision Cognitive Neurology at NYU
Research Interest
Dr. Boutajangout is a Research Associate Professor friendly Neurology and Neuroscience & Physiology promote Psychiatry. He serves as the gaffer of the Neurodegeneration and Drug Hunt down Program within the Center for Cerebral Neurology at NYU. His research focuses on a new derivative peptide be advantageous to Amyloid beta for use as immunotherapy or vaccine t
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Abstract
Harnessing the immune system to clear protein aggregates is emerging as a promising approach to treat various neurodegenerative diseases. In Alzheimer's disease (AD), several clinical trials are ongoing using active and passive immunotherapy targeting the amyloid-β (Aβ) peptide. Limited emphasis has been put into clearing tau/tangle pathology, another major hallmark of the disease. Recent findings from the first Aβ vaccination trial suggest that this approach has limited effect on tau pathology and that Aβ plaque clearance may not halt or slow the progression of dementia in individuals with mild-to-moderate AD. To assess within a reasonable timeframe whether targeting tau pathology with immunotherapy could prevent cognitive decline, we developed a new model with accelerated tangle development. It was generated by crossing available strains that express all six human tau isoforms and the ML presenilin mutation. Here, we show that this unique approach completely prevents sev