Research Progress on Natural Plant Molecules in Regulating the Blood–Brain Barrier in Alzheimer’s Disease

Abstract

Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder. With the aging population and the continuous development of risk factors associated with AD, it will impose a significant burden on individuals, families, and society. Currently, commonly used therapeutic drugs such as Cholinesterase inhibitors, N-methyl-D-aspartate antagonists, and multiple AD pathology removal drugs have been shown to have beneficial effects on certain pathological conditions of AD. However, their clinical efficacy is minimal and they are associated with certain adverse reactions. Furthermore, the underlying pathological mechanism of AD remains unclear, posing a challenge for drug development. In contrast, natural plant molecules, widely available, offer multiple targeting pathways and demonstrate inherent advantages in modifying the typical pathologic features of AD by influencing the blood–brain barrier (BBB). We provide a comprehensive review of recent in vivo and in vitro studies on natural plant molecules that impact the BBB in the treatment of AD. Additionally, we analyze their specific mechanisms to offer novel insights for the development of safe and effective targeted drugs as well as guidance for experimental research and the clinical application of drugs for the prevention and treatment of AD.

Composite of KLVFF-Transthyretin-Penetratin and Manganese Dioxide Nanoclusters: A Multifunctional Agent against Alzheimer’s β-Amyloid Fibrillogenesis

“…Alzheimer’s disease (AD) stands as one of the most prevalent neurodegenerative diseases, with clinical characteristics of memory deficit, cognition impairment, communicative decline, emotional disorder, and disabling behavior. It is a complex and multifactorial disease with pathological mechanisms such as amyloid β-protein (Aβ) aggregation, tau protein hyperphosphorylation, neuroinflammation, and synaptic dysfunction [ 1 , 2 ]. One of the pathologic features of AD is extracellular amyloid plaque deposition, resulting from the gradual accumulation and aggregation of amyloid β-protein (Aβ) in the cerebrum [ 3 ].…”