Regulation of beta‐amyloid for the treatment of Alzheimer&apos;s disease: Research progress of therapeutic strategies and bioactive compounds

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Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease that is difficult to treat. Extracellular amyloid is the principal pathological criterion for the diagnosis of AD. Amyloid β (Aβ) interacts with various receptor molecules on the plasma membrane and mediates a series of signaling pathways that play a vital role in the occurrence and development of AD. Research on receptors that interact with Aβ is currently ongoing. Overall, there are no effective medications to treat AD. In this review, we first discuss the importance of Aβ in the pathogenesis of AD, then summarize the latest progress of Aβ‐related targets and compounds. Finally, we put forward the challenges and opportunities in the development of effective AD therapies.

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Alzheimer Disease: An Update on Pathobiology and Treatment Strategies

Justin M. Long, David Holtzman (2019)

Alzheimer disease (AD) is a heterogeneous disease with a complex pathobiology. The presence of extracellular amyloid-β deposition as neuritic plaques and intracellular accumulation of hyperphosphorylated tau as neurofibrillary tangles remain the primary neuropathologic criteria for AD diagnosis. However, a number of recent fundamental discoveries highlight important pathological roles for other critical cellular and molecular processes. Despite this, no disease modifying treatment currently exists and numerous phase 3 clinical trials have failed to demonstrate benefit. We review here recent advances in our understanding of AD pathobiology and discuss current treatment strategies, highlighting recent clinical trials and opportunities for developing future disease modifying therapies.

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2020 Alzheimer's disease facts and figures

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Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?

Fangda Leng, Paul Edison (2021)

Alzheimer disease (AD) is the most common form of neurodegenerative disease, estimated to contribute 60-70% of all cases of dementia worldwide. According to the prevailing amyloid cascade hypothesis, amyloid-β (Aβ) deposition in the brain is the initiating event in AD, although evidence is accumulating that this hypothesis is insufficient to explain many aspects of AD pathogenesis. The discovery of increased levels of inflammatory markers in patients with AD and the identification of AD risk genes associated with innate immune functions suggest that neuroinflammation has a prominent role in the pathogenesis of AD. In this Review, we discuss the interrelationships between neuroinflammation and amyloid and tau pathologies as well as the effect of neuroinflammation on the disease trajectory in AD. We specifically focus on microglia as major players in neuroinflammation and discuss the spatial and temporal variations in microglial phenotypes that are observed under different conditions. We also consider how these cells could be modulated as a therapeutic strategy for AD.

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Author and article information

Contributors

Weimin Qiu: (View ORCID Profile)

Haopeng Sun: (View ORCID Profile)

Journal

Title: Medicinal Research Reviews

Abbreviated Title: Medicinal Research Reviews

Publisher: Wiley

ISSN (Print): 0198-6325

ISSN (Electronic): 1098-1128

Publication date Created: July 2023

Publication date (Electronic): March 21 2023

Publication date (Print): July 2023

Volume: 43

Issue: 4

Pages: 1091-1140

Affiliations

[1 ] Department of Medicinal Chemistry School of Pharmacy, China Pharmaceutical University Nanjing China

[2 ] Department of Natural Medicinal Chemistry China Pharmaceutical University Nanjing China

[3 ] Department of Natural Medicinal Chemistry, Jiangsu Food and Pharmaceuticals Science College Institute of Food and Pharmaceuticals Research Jiangsu Huaian China

[4 ] Department of Pharmacology, School of Basic Medicine Qingdao University Qingdao China