Cuscutae Japonicae Semen Ameliorates Memory Dysfunction by Rescuing Synaptic Damage in Alzheimer’s Disease Models

Abstract

Alzheimer’s disease (AD) is the most common type of dementia in the elderly. It is characterized by the accumulation of amyloid-beta (Aβ) and progressive cognitive impairment. To alleviate the symptoms of AD, functional foods and nutrients have been used for centuries. In this study, we investigated whether Cuscutae Japonicae Semen (CJS), a medicinal food traditionally used in East Asia, has effects on memory improvement and synapse protection in AD. We orally administered CJS to 5x familiar AD (5xFAD) transgenic mice and performed the Morris water maze test. The results showed that CJS treatment ameliorated the decline of memory function. Then, we demonstrated that CJS attenuated the degeneration of pre- and post-synaptic proteins in the hippocampi of 5xFAD mice. To demonstrate the effects of CJS in vitro, we treated Aβ in primary neuronal culture with CJS and observed that CJS rescued the loss of functional synapses. The protective effects of CJS on the synapse were due to the inhibition of activated caspase-3 expression. Additionally, CJS inhibited the phosphorylation of glycogen synthase kinase-3β and tau proteins, which contribute to synaptic dysfunction. Taken together, our results suggest that CJS is efficient in alleviating memory loss by rescuing caspase-3-mediated synaptic damage in AD treatment.

Lactobacillus plantarum PS128 prevents cognitive dysfunction in Alzheimer’s disease mice by modulating propionic acid levels, glycogen synthase kinase 3 beta activity, and gliosis

“…The MWM task was used to evaluate the spatial learning and memory abilities of mice as previously described [29]. The MWM assay consisted of four stages: pretraining (day 34), training (days [35][36][37][38], testing (day 39), and probe (day 40). The swimming ability of the mice was tested on day 34.…”

“…Based on these data, PS128 prevented icv-STZ-induced gliosis in 3 × Tg-AD mice. Synaptic proteins, including postsynaptic density protein 95 (PSD95) and synaptophysin, play critical roles in synaptic plasticity and cognitive function [37,38]. Therefore, the levels of PSD95 and synaptophysin proteins were examined using western blot analyses.…”

The novel anti-neuroinflammatory functional food CCL01, a mixture of Cuscuta seed extracts and Lactobacillus paracasei NK112

“…Previous studies reported that the individual components of CCL01, Cuscuta seeds and Lactobacillus paracasei NK112 (NK112), reduced the production levels of IL-6 and TNF-α and expression levels of the proteins iNOS and COX-2 via regulating NF-κB activation. 10–12,23 However, the anti-neuroinflammatory effects of the mixture with a synergic effect on LPS-induced BV2 microglia have not been reported. Thus, our data supported the anti-neuroinflammatory effects of CCL01, which was shown in our previous study to be a potential enhancer of memory function.…”

“…9 Indeed, each component showed ameliorative effects on models of neurological disorders such as depression and cognitive impairment. 10–12 Therefore, our study suggests a new focus on the microbiota–gut–brain axis with respect to the central nervous system as a new potential pathway that may mediate neurodegenerative pathogenesis ( i.e. , depression and cognitive impairment) in response to lipopolysaccharide (LPS).…”

Cuscutae semen alleviates CUS-induced depression-like behaviors in mice via the gut microbiota-neuroinflammation axis

“…plant, contains high contents of flavonoids, polysaccharides, alkaloids, and resin glycosides. Several studies have shown that CS has various biological activities pertaining to neuroprotection (Zhen et al, 2006), anti-neuroinflammation (Kang et al, 2014), the rescue of synaptic damage (Ju et al, 2019), and the alleviation of oxidative stress (Lin et al, 2018). Seok Y et al reported that CS extract suppresses the inflammatory response by inhibiting the expression of cyclooxygenase-2 (COX-2), downregulating the transcription levels of TNF-α, IL-1β, and IL-6, and contributing to the nuclear translocation of nuclear factor kappa B (NF-κB) P65 in activated microglia (Kang et al, 2014).…”