Abstract
Alzheimer’s disease (AD) is a neurodegenerative disease that causes memory loss, cognitive decline, and eventually dementia. The etiology of AD and its pathological mechanisms remain unclear due to its complex pathobiology. At the same time, the number of patients with AD is increasing worldwide. However, no therapeutic agents for AD are currently available for definitive care. Several phase 3 clinical trials using agents targeting amyloid β (Aβ) and its related molecules have failed, with the exception of aducanumab, an anti-Aβ monoclonal antibody (mAb), clinically approved by the US Food and Drug Administration in 2021, which could be modified for AD drug development due to controversial approval. Neurofibrillary tangles (NFTs) composed of tau rather than senile plaques composed of Aβ are correlated with AD pathogenesis. Moreover, Aβ and tau pathologies initially proceed independently. At a certain point in the progression of AD symptoms, the Aβ pathology is involved in the alteration and spreading of the tau pathology. Therefore, tau-targeting therapies have attracted the attention of pharmaceutical scientists, as well as Aβ-targeting therapies. In this review, I introduce the implementations and potential of AD immunotherapy using intravenously administered anti-tau and anti-receptor bispecific mAbs. These cross the blood-brain barrier (BBB) based on receptor-mediated transcytosis and are subsequently cleared by microglia based on Fc-mediated endocytosis after binding to tau and lysosomal degradation.
Highlights
Medicinal remedies provide long-term health benefits to humans
Introduce immunotherapy using intravenously administered anti-tau monoclonal antibody (mAb) to spective review, I introduce immunotherapy using intravenously administered anti-tau be delivered into the brain based on receptor-mediated transcytosis, using a mAbs to be delivered into the brain based on receptor-mediated transcytosis, bispecific strategy
It is suggested that tau plays a vital role in Alzheimer’s disease (AD) pathology, amyloid β (Aβ) is involved in it due to the existence of familial AD accompanied by mutations in APP, presenilin 1, or presenilin 2
Summary
Medicinal remedies provide long-term health benefits to humans. treatments for several important diseases have yet to be developed, including neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Almost all clinical trials for AD, including phase 3 studies using pharmaceutical agents targeting amyloid β (Aβ) and its related molecules, such as β-secretase 1 and γ-secretase, have failed. Many pharmaceutical companies have abandoned efforts to develop AD drugs [1]. An analysis of several clinical trial failures and AD research has suggested alternative strategies for the targeting of tau, in addition to Aβ. Pharmaceutics 2022, 14, 411 analysis of several clinical trial failures and AD research has suggested alternative strategies for the targeting of tau, in addition to Aβ. AD symptom progression pathology at a spreading certain point of AD symptom [4].ofMoreover, the presence of [4].
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