scholarly journals M5. Beta Amyloid Level is not Elevated in Elderly Patients With Schizophrenia: Are There Potential Neuroprotective Effects of Antipsychotics on Beta-Amyloid Pathology?

2017 ◽  
Vol 43 (suppl_1) ◽  
pp. S212-S212
Author(s):  
Jun Ku Chung ◽  
Shinichiro Nakajima ◽  
Eric Plitman ◽  
Fernando Caravaggio ◽  
Philip Gerretsen ◽  
...  
Keyword(s):  
Elderly Patients ◽  
Beta Amyloid ◽  
Neuroprotective Effects ◽  
Amyloid Pathology

The neuroprotective effects of flupirtine and beta-amyloid induced memory impairment

2011 ◽  
Author(s):  
Matthew Jefferson ◽  
Sara Smeltzer ◽  
Jeffery L. McMillin ◽  
Caitlin C. Henry ◽  
Brittney M. Klauser ◽  
...  
Keyword(s):  
Memory Impairment ◽  
Beta Amyloid ◽  
Neuroprotective Effects

Neuroprotective effects of sigma-1 receptor agonists against beta-amyloid-induced toxicity

Neuroreport ◽  
2005 ◽  
Vol 16 (11) ◽  
pp. 1223-1226 ◽  
Author(s):  
Agostino Marrazzo ◽  
Filippo Caraci ◽  
Elisa Trovato Salinaro ◽  
Tsung-Ping Su ◽  
Agata Copani ◽  
...  
Keyword(s):  
Beta Amyloid ◽  
Neuroprotective Effects ◽  
Sigma 1 Receptor ◽  
Receptor Agonists ◽  
Sigma 1

scholarly journals Fecal Microbiota Transplantation Decreases Amyloid Load and Improves Cognition in Alzheimer’s

2019 ◽  
Author(s):  
Shalini Elangovan ◽  
Thomas J Borody ◽  
R M Damian Holsinger
Keyword(s):  
Alzheimer’S Disease ◽  
Recognition Memory ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Therapeutic Effects ◽  
Wild Type ◽  
Neuroprotective Effects ◽  
Amyloid Pathology ◽  
Amyloid Load ◽  
Old Mice

AbstractThe efficacy of fecal microbiota transplantation (FMT) in Alzheimer’s disease has yet to be investigated. Here, we show that FMT is capable of providing neuroprotective effects in two groups of treated 5xFAD Alzheimer’s mice, old transgenic (Tg) mice fed fecal slurry from healthy, wild-type donors of similar age (Old Tg-FO) and old mice fed fecal slurry from younger healthy, wild-type donors (Old Tg-FY). Improved spatial and recognition memory in Old Tg-FY and enhanced recognition memory in Old Tg-FO were observed when compared to Old Tg-Control mice given saline. Crucially, there was significant decreases in cortical Aβ loading in all treated mice, demonstrating the therapeutic effects of FMT in improving cognition and reducing amyloid pathology in AD brains.One Sentence SummaryFecal microbial transplants reduce amyloid pathology and improve cognition in Alzheimer’s mice.

Piper sarmentosum Roxb. Attenuates Beta Amyloid (Aβ)-Induced Neurotoxicity Via the Inhibition of Amyloidogenesis and Tau Hyperphosphorylation in SH-SY5Y Cells

2021 ◽  
Vol 18 (1) ◽  
pp. 80-87
Author(s):  
Elaine W.L. Chan ◽  
Emilia T.Y. Yeo ◽  
Kelly W.L. Wong ◽  
Mun L. See ◽  
Ka Y. Wong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Beta Amyloid ◽  
Mechanistic Study ◽  
Tau Hyperphosphorylation ◽  
Neuroprotective Effects ◽  
Human Neuroblastoma ◽  
Hexane Extracts ◽  
Anti Oxidant ◽  
Amyloid Aβ

Background: In Alzheimer’s disease, accumulation of beta amyloid (Aβ) triggers amyloidogenesis and hyperphosphorylation of tau protein leading to neuronal cell death. Piper sarmentosum Roxb. (PS) is a traditional medicinal herb used by Malay to treat rheumatism, headache and boost memory. It possesses various biological effects, such as anti-cholinergic, anti-inflammatory, anti-oxidant and anti-depressant-like effects. Objective: The present study aimed to investigate neuroprotective properties of PS against Aβ-induced neurotoxicity and to evaluate its potential mechanism of action. Methods: Neuroprotective effects of hexane (HXN), dichloromethane (DCM), ethyl acetate (EA) and methanol (MEOH) extracts from leaves (L) and roots (R) of PS against Aβ-induced neurotoxicity were investigated in SH-SY5Y human neuroblastoma cells. Cells were pre-treated with PS for 24 h followed by 24 h of induction with Aβ. The neuroprotective effects of PS were studied using cell viability and cellular reactive oxygen species (ROS) assays. The levels of extracellular Aβ and tau proteins phosphorylated at threonine 231 (pT231) were determined. Gene and protein expressions were assessed using qRT-PCR analyses and western blot analyses, respectively. Results: Hexane extracts of PS (LHXN and RHXN) protected SH-SY5Y cells against Aβ-induced neurotoxicity, and decreased levels of extracellular Aβ and phosphorylated tau (pT231). Although extracts of PS inhibited Aβ-induced ROS production, it was unlikely that neuroprotective effects were simply due to the anti-oxidant capacity of PS. Further, mechanistic study suggested that the neuroprotective effects of PS might be due to its capability to regulate amyloidogenesis through the downregulation of BACE and APP. Conclusion: These findings suggest that hexane extracts of PS confer neuroprotection against Aβ- induced neurotoxicity in SH-SY5Y cells by attenuating amyloidogenesis and tau hyperphosphorylation. Due to its neuroprotective properties, PS might be a potential therapeutic agent for Alzheimer’s disease.

scholarly journals Bajijiasu Ameliorates β-Amyloid-Triggered Endoplasmic Reticulum Stress and Related Pathologies in an Alzheimer’s Disease Model

2018 ◽  
Vol 46 (1) ◽  
pp. 107-117 ◽  
Author(s):  
Ting-Ting Xu ◽  
Yang Zhang ◽  
Jia-Yang He ◽  
Dan Luo ◽  
Yi Luo ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Western Blotting ◽  
Disease Model ◽  
Beta Amyloid ◽  
Amyloid Peptide ◽  
Neuroprotective Effects ◽  
Beneficial Effects ◽  
Y Maze ◽  
Improved Learning

Background/Aims: Alzheimer disease (AD) is a common neurodegenerative disease that is characterized by the deposition of beta-amyloid peptide and formation of intracellular neurofibrillary tangles. Due to the failure of various clinical trials of novel drugs for AD, effective drugs for AD treatment are urgently required. Methods: In this study, we used the classic APP/PS1 mouse model to explore the neuroprotective effects of a new compound, bajijiasu, and the mechanisms involved. Behavioral tests and western blotting were performed to assess the beneficial effects of bajijiasu in APP/PS1 mice. Results: Morris water maze and Y-maze test results showed that oral administration of bajijiasu (35 mg/kg/day and 70 mg/kg/day) improved learning and memory abilities in APP/PS1 mice. Bajijiasu reduced ROS and MDA levels in both the hippocampus and cortex. Moreover, western blotting results showed that bajijiasu protected neurons from apoptosis, elevated the expression levels of neurotrophic factors, and alleviated endoplasmic reticulum stress in both the hippocampus and cortex. Conclusion: These results indicate that the mechanisms underlying the effects of bajijiasu on AD might be related to beta-amyloid-downstream pathologies, particularly endoplasmic reticulum stress.

scholarly journals Salidroside Attenuates Cognitive Dysfunction in Senescence-Accelerated Mouse Prone 8 (SAMP8) and Modulating Inflammation on the Gut-brain Axis

2020 ◽  
Author(s):  
Zeping Xie ◽  
Hui Lu ◽  
Sixia Yang ◽  
Yi Zeng ◽  
Wei Li ◽  
...  
Keyword(s):  
Western Blot ◽  
Therapeutic Effect ◽  
Memory Loss ◽  
Field Tests ◽  
Beta Amyloid ◽  
Illumina Miseq ◽  
Peripheral Circulation ◽  
Neuroprotective Effects ◽  
Multiplex Immunoassay ◽  
Significant Difference

Abstract Background Alzheimer’s disease (AD), as the most prime cause of dementia, is a fatal neurodegenerative disease characterized by progressive cognitive decline and memory loss. However, A range of therapeutic approaches have shown unsatisfactory outcomes in clinical setting. Thus, it is critical to develop alternative therapies for the treatment of AD. Salidroside(SAL), a herb-derived phenylpropanoid glycoside compound, has been shown to attenuate LPS-induced cognitive impairment. However, the mechanism underlying its neuroprotective effects remains unclear. Here we show a therapeutic effect of SAL in a reliable and stable mouse model of AD, Senescence-Accelerated Mice Prone 8 (SAMP8).Methods SAMP8 were treated with salidroside, donepezil or saline, cognitive behavioral impairments were assessed using the Morris water maze, Y-maze, and open-field tests. Fecal samples were collected and analyzed by 16S rRNA sequencing, performed on the Illumina MiSEq. Brain samples were analyzed by immunohistochemistry and western blot to detect Beta Amyloid 1–42 deposition. Activation in microglia and neuroinflammatory cytokines was detected by immunofluorescence, Western blot and qPCR. Serum was analyzed by a Mouse High Sensitivity T Cell Magnetic Bead Panel and performed on the Luminex-MAGPIX multiplex immunoassay system.Results Our results suggested that SAL effectively alleviated hippocampus-dependent memory impairment in SAMP8, and showed no significant difference compared with the donepezil-administration group. SAL significantly (1) reduced toxic beta-amyloid (Abeta) 1–42 deposition; (2) reduced activation of microglia and attenuated proinflammatory factors, IL-1β, IL-6, and TNF-α, in the brain; (3) improved the gut barrier integrity and modified the gut microbiota (reversed the ratio of Bacteroidetes to Firmicutes, and eliminated Clostridiales and Streptococcaceae, which may have been associated with cognitive deficits); and (4) decreased the levels of proinflammatory cytokines in the peripheral circulation, IL-1α, IL-6, IL-17A and IL-12 in particular, according to a multiplex immunoassay.Conclusion In summary, SAL reversed AD-related changes in SAMP8 potentially through the regulation of the microbiota-gut-brain axis and by modulating inflammation in both peripheral circulation and central nervous system. Our results strongly suggest a therapeutic effect of SAL on cognition-related changes in SAMP8 and highlight its value as a potential source for drug development.

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