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2000
Volume 23, Issue 1
  • ISSN: 1389-5575
  • E-ISSN: 1875-5607

Abstract

Alzheimer’s disease or senile dementia is principally acknowledged by the gradual accumulation of neurotoxic amyloid- β protein in the brain and is considered as the initial event of the phenomenon of this asymptomatic ailment. It prompts the decline in cognitive performance, standard psychiatric functioning, and neuronal transmission across the brain. Significant inferences were withdrawn by utilizing the recently introduced disease-modifying anti- amyloid- β immunotherapy developed after performing the clinical and preclinical controlled trials to cure the neurodegenerative malady. This strategy is worthwhile because of the clinical relevance and specific targeted approach that exhibited the quenched immunotherapeutic effects and encouraged clinical findings. In vitro fabricated, anti- amyloid- β recombinant monoclonal antibodies are passively employed to promote clearance and antagonize the aggregation and synthesis of neurotoxic and degenerative aggregates of amyloid-β. Thus, passive immunotherapy has an adequate impact on treating this disorder, and currently, some other monoclonal pharmacological molecules are under clinical trials to defeat this severe exacerbation with more efficacy and clinical benefits. This review compendiously discusses the anti-amyloid-β immunotherapy, which will provide a more proficient framework to be employed as a potential therapeutic approach.

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/content/journals/mrmc/10.2174/1389557522666220524090354
2023-01-01
2024-12-27
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