Cognitive-enhancing effects of hydrolysate of polygalasaponin in SAMP8 mice

Xu, Pan; Xu, Shuping; Wang, Kezhu; Lü, Cong; Zhang, Hongxia; Pan, Rui‐Le; Chang, Qi; Yang, Yanmin; Li, Yinghui; Liu, Xinmin

doi:10.1631/jzus.b1500321

Cited by 14 publications

(11 citation statements)

References 53 publications

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“…These findings are in line with other studies showing that SAMP8 mice displayed a significant increase in escape latency time since the first day of training as compared with SAMR1 mice, while no significant difference was observed among training days [38, 39].…”

Section: Resultssupporting

confidence: 92%

High Levels of β-Amyloid, Tau, and Phospho-Tau in Red Blood Cells as Biomarkers of Neuropathology in Senescence-Accelerated Mouse

Piccarducci

Pietrobono

Pellegrini

et al. 2019

Oxidative Medicine and Cellular Longevity

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Alzheimer’s Disease (AD) is the most common Neurodegenerative Disease (ND), primarily characterised by neuroinflammation, neuronal plaques of β-amyloid (Aβ), and neurofibrillary tangles of hyperphosphorylated tau. α-Synuclein (α-syn) and its heteroaggregates with Aβ and tau have been recently included among the neuropathological elements of NDs. These pathological traits are not restricted to the brain, but they reach peripheral fluids as well. In this sense, Red Blood Cells (RBCs) are emerging as a good model to investigate the biochemical alterations of aging and NDs. Herein, the levels of homo- and heteroaggregates of ND-related proteins were analysed at different stages of disease progression. In particular, a validated animal model of AD, the SAMP8 (Senescence-Accelerated Mouse-Prone) and its control strain SAMR1 (Senescence-Accelerated Mouse-Resistant) were used in parallel experiments. The levels of the aforementioned proteins and of the inflammatory marker interleukin-1β (IL-1β) were examined in both brain and RBCs of SAMP8 and SAMR1 at 6 and 8 months. Brain Aβ, tau, and phospho-tau (p-tau) were higher in SAMP8 mice than in control mice and increased with AD progression. Similar accumulation kinetics were found in RBCs, even if slower. By contrast, α-syn and its heterocomplexes (α-syn-Aβ and α-syn-tau) displayed different accumulation kinetics between brain tissue and RBCs. Both brain and peripheral IL-1β levels were higher in SAMP8 mice, but increased sooner in RBCs, suggesting that inflammation might initiate at a peripheral level before affecting the brain. In conclusion, these results confirm RBCs as a valuable model for monitoring neurodegeneration, suggesting peripheral Aβ, tau, and p-tau as potential early biomarkers of AD.

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Section: Resultssupporting

confidence: 92%

High Levels of β-Amyloid, Tau, and Phospho-Tau in Red Blood Cells as Biomarkers of Neuropathology in Senescence-Accelerated Mouse

Piccarducci

Pietrobono

Pellegrini

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…Aberrations in the lower symmetrical regions in the DMN (such as the precuneus and fusiform) could be the principal reason for memory decline. These regions play an important role in visual information processing of AD patients (Chang et al, 2015;Xu et al, 2016). Buckner et al (2005) also observed that disruption of the medial temporal lobe contributed to memory impairment.…”

Section: Fig 2 Analysis Of Vmhc Resultsmentioning

confidence: 93%

Interhemispheric functional connectivity for Alzheimer’s disease and amnestic mild cognitive impairment based on the triple network model

Liao

Tan

Qiu

et al. 2018

J. Zhejiang Univ. Sci. B

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The purpose of this study was to explore the differences in interhemispheric functional connectivity in patients with Alzheimer's disease (AD) and amnestic mild cognitive impairment (aMCI) based on a triple network model consisting of the default mode network (DMN), salience network (SN), and executive control network (ECN). The technique of voxel-mirrored homotopic connectivity (VMHC) analysis was applied to explore the aberrant connectivity of all patients. The results showed that: (1) the statistically significant connections of interhemispheric brain regions included DMN-related brain regions (i.e. precuneus, calcarine, fusiform, cuneus, lingual gyrus, temporal inferior gyrus, and hippocampus), SN-related brain regions (i.e. frontoinsular cortex), and ECN-related brain regions (i.e. frontal middle gyrus and frontal inferior); (2) the precuneus and frontal middle gyrus in the AD group exhibited lower VMHC values than those in the aMCI and healthy control (HC) groups, but no significant difference was observed between the aMCI and HC groups; and (3) significant correlations were found between peak VMHC results from the precuneus and Mini Mental State Examination (MMSE) and Montreal Cognitive Scale (MOCA) scores and their factor scores in the AD, aMCI, and AD plus aMCI groups, and between the results from the frontal middle gyrus and MOCA factor scores in the aMCI group. These findings indicated that impaired interhemispheric functional connectivity was observed in AD and could be a sensitive neuroimaging biomarker for AD. More specifically, the DMN was inhibited, while the SN and ECN were excited. VMHC results were correlated with MMSE and MOCA scores, highlighting that VMHC could be a sensitive neuroimaging biomarker for AD and the progression from aMCI to AD.

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“…Besides, the content of phosphorylated and non-phosphorylated NMDAR subunits in the hippocampus of AD patients are reduced (Sze et al, 2001). Consistently, in SAMP8 mice or AD models injected with Aβ 25-35 or Aβ 1-42 , the expression of NMDAR1, NMDAR2A and NMDAR2B were decreased markedly in the hippocampus or cortex (K. W. Chang et al, 2020; K. Wang et al, 2018; Xu et al, 2016). Moreover, it has been demonstrated that ketamine, a noncompetitive NMDAR antagonist, could ameliorate the impaired learning and memory of developing mice induced by repetitive mechanical stress, and the mechanism may be associated with the increased hippocampal BDNF expression (C. H. Chang, Su, & Gean, 2018; Peng, Zhang, Wang, Ren, & Zhang, 2011).…”

Section: Discussionmentioning

confidence: 67%

Impaired learning and memory ability induced by a bilaterally hippocampal injection of streptozotocin in mice: involved with the adaptive changes of synaptic plasticity

Chen

Gao

et al. 2020

Preprint

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BackgroundAlzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline, psychiatric symptoms and behavioral disorders, resulting in disability and loss of self-sufficiency.ObjectiveTo establish an AD mice model, investigate the behavioral performance, and explore the potential mechanism.MethodsStreptozotocin (STZ, 3 mg/kg) was microinjected bilaterally into the dorsal hippocampus of C57BL /6 mice to establish the AD model. Behavioral changes (anhedonia and despair, balance and motor coordination, locomotion, and learning and memory) were examined and the serum concentrations of insulin and nesfatin-1 were measured by ELISA. The activation of hippocampal microglia was assessed by immunohistochemistry and the protein expression of several molecular associated with the regulation of synaptic plasticity in the hippocampus and the prefrontal cortex (PFC) was detected via western blotting.ResultsThe STZ model mice showed a slower bodyweight gain and higher serum concentration of insulin and nesfatin-1. Although there was no significant difference between groups with regard to the ability of balance and motor coordination, the model mice presented a decline of spontaneous movement and exploratory behavior, together with an impairment of learning and memory ability. Increased activated microglia was aggregated in the hippocampal dentate gyrus of model mice. Moreover, the protein expression of NMDAR2A, NMDAR2B, SynGAP, PSD95, BDNF, and p-β-catenin/β-catenin were remarkably decreased in the hippocampus and the PFC of model mice, and the expression of p-GSK-3β (ser9)/GSK-3β were reduced in the hippocampus.ConclusionA bilateral hippocampal microinjection of STZ could successfully duplicate an AD mice model, as indicated by the impaired learning and memory and the alternated synaptic plasticity, together with the hyperactive inflammatory response in the hippocampus and the imbalanced abundance of serum insulin and nesfatin-1. Apart from these, the mechanism might be associated with the imbalanced expression of the key proteins of Wnt signaling pathway in the hippocampus and the PFC.Graphical abstract

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Cognitive-enhancing effects of hydrolysate of polygalasaponin in SAMP8 mice

Cited by 14 publications

References 53 publications

High Levels of β-Amyloid, Tau, and Phospho-Tau in Red Blood Cells as Biomarkers of Neuropathology in Senescence-Accelerated Mouse

High Levels of β-Amyloid, Tau, and Phospho-Tau in Red Blood Cells as Biomarkers of Neuropathology in Senescence-Accelerated Mouse

Interhemispheric functional connectivity for Alzheimer’s disease and amnestic mild cognitive impairment based on the triple network model

Impaired learning and memory ability induced by a bilaterally hippocampal injection of streptozotocin in mice: involved with the adaptive changes of synaptic plasticity

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