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Alzheimerʼs disease (AD) is a critical neurodegenerative disease that manifests as progressive intellectual decline and is pathologically characterized by a progressive loss of neurons in the brain. Despite extensive research on this topic, the pathogenesis of AD is not fully understood, while the beta-amyloid (A β) hypothesis remains the dominant one and only a few symptomatic drugs are approved for the treatment of AD. Ginseng has been widely reported as an effective herbal medicine for the treatment of neurodegenerative diseases such as dementia. Therefore, we explore the protective effects of ginseng in AD by a network pharmacological approach based on the pathogenesis of A β. Twenty-one major ginsenosides are screened based on ultraperformance liquid chromatography-mass spectrometry/mass spectrometry (HPLC-MS/MS) data. Among them, MAPK8, MAPK9, BACE1, FLT1, CDK2, and CCR5 are the core targets. By molecular docking and validation with the in vitro cell model APPswe-SH-SY5Y, we find that ginsenosides Rg3 and Ro have good neuroprotective effects and can reduce the expression of A β1 – 42 in APPswe-SH-SY5Y. Finally, through RT-qPCR experiment, we find that ginsenoside Rg3 targeted MAPK8, FLT1, and CCR5, while ginsenoside Ro targeted MAPK8, MAPK9, FLT1, and CCR5 for its potential anti-AD efficacy. [ABSTRACT FROM AUTHOR]

Emerging treatments for spinal cord damage. Dementia, Alzheimer's, Parkinson's – Confusions, myths and tips. An update on Alzheimer's disease. Integration of Traditional Chinese medicine and Western medicine in cancer treatment. TCM's integration into modern health system. [ABSTRACT FROM AUTHOR]

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The article presents a study, conducted by researcher A. Gonzalo-Ruiz and colleagues, which focuses on cerebral cortex cholinergic fibers loss. The influence of diet and age on the effects of intracerebral injection of beta-amyloid peptide (Abeta1-40) in vehicle phosphate-buffered saline (PBS) and on the effects of vehiclealone on cholinergic fibers of the cerebral cortex was studied in rats. In all diet groups the loss of cholinergic fibers caused by Abeta as compared to that caused by PBS injection was significantly greater in aged rats in comparison with that observed in the young animals. Gonzaloruiz and colleagues published their study in the "Journal of Chemical Neuroanatomy."

The article cites a study in which investigators have chronicled the modification of amyloid beta peptide-induced cholinergic fibers loss in the cerebral cortex by a high-lipid diet and by age. Researcher A. Gonzalo-Ruiz and colleagues said that the influence of diet and age on the effects of intracerebral injection of beta-amyloid peptide (Abeta1-40) in vehicle phosphate-buffered saline and on the effects of vehicle alone on cholinergic fibers of the cerebral cortex was studied in rats. Gonzaloruiz and colleagues published their study in the "Journal of Chemical Neuroanatomy."

A cross-sectional study involving 1,219 cognitively healthy elderly people (+65 years) who were participants in a community-based multiethnic cohort study identified an inverse association between omega-3 fatty acids and beta-amyloid (Ab). Information on dietary intake was obtained 1.2 years, on average, before Ab assay. The associations of plasma Ab40 and Ab42 levels and dietary intake of saturated fatty acid, monounsaturated fatty acid, omega-3 polyunsaturated fatty acid (PUFA), omega-6 PUFA, vitamin E, vitamin C, beta-carotene, vitamin B(12), folate, and vitamin D were examined. Results found omega-3 fatty acids were a strong predictor of Ab42, less so with Ab40. Data suggests that higher dietary omega-3 fatty acid intake may be associated with lower plasma levels of Ab42, a reduced risk of incident AD and slower cognitive decline. [ABSTRACT FROM AUTHOR]