Magnolol upregulates CHRM1 to attenuate Amyloid-β-triggered neuronal injury through regulating the cAMP/PKA/CREB pathway

Background: Neprilysin (NEP) cleaves amyloid-β 1–42 (Aβ42) in the brain. Hence, we aimed to elucidate the effect of NEP on Aβ42 in cerebrospinal fluid (CSF) and on in vivo brain amyloid load using amyloid positron emission tomography (PET) with [11C]PiB (Pittsburgh compound B). In addition, associations with the biomarkers for neuronal injury, CSF-tau and FDG-PET, were investigated. Methods: Associations were calculated using global and voxel-based (SPM8) linear regression analyses in the same cohort of 23 highly characterized Alzheimer’s disease patients. Results: CSF-NEP was significantly inversely associated with CSF-Aβ42 and positively with the extent of neuronal injury as measured by CSF-tau and FDG-PET. Conclusions: Our results on CSF-NEP are compatible with the assumption that local degradation, amongst other mechanisms of amyloid clearance, plays a role in the development of Alzheimer’s pathology. In addition, CSF-NEP is associated with the extent and the rate of neurodegeneration.

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Neuropharmacological Effects of Quercetin: A Literature-Based Review

Frontiers in Pharmacology ◽

10.3389/fphar.2021.665031 ◽

2021 ◽

Vol 12 ◽

Author(s):

Md. Shahazul Islam ◽

Cristina Quispe ◽

Rajib Hossain ◽

Muhammad Torequl Islam ◽

Ahmed Al-Harrasi ◽

...

Keyword(s):

Neurodegenerative Diseases ◽

Neuroprotective Effect ◽

Animal Experiments ◽

Amyloid Β ◽

Neuronal Injury ◽

Amyloid Β Peptide ◽

Protective Effects ◽

Neuroprotective Effects

Quercetin (QUR) is a natural bioactive flavonoid that has been lately very studied for its beneficial properties in many pathologies. Its neuroprotective effects have been demonstrated in many in vitro studies, as well as in vivo animal experiments and human trials. QUR protects the organism against neurotoxic chemicals and also can prevent the evolution and development of neuronal injury and neurodegeneration. The present work aimed to summarize the literature about the neuroprotective effect of QUR using known database sources. Besides, this review focuses on the assessment of the potential utilization of QUR as a complementary or alternative medicine for preventing and treating neurodegenerative diseases. An up-to-date search was conducted in PubMed, Science Direct and Google Scholar for published work dealing with the neuroprotective effects of QUR against neurotoxic chemicals or in neuronal injury, and in the treatment of neurodegenerative diseases. Findings suggest that QUR possess neuropharmacological protective effects in neurodegenerative brain disorders such as Alzheimer’s disease, Amyloid β peptide, Parkinson’s disease, Huntington's disease, multiple sclerosis, and amyotrophic lateral sclerosis. In summary, this review emphasizes the neuroprotective effects of QUR and its advantages in being used in complementary medicine for the prevention and treatment o of different neurodegenerative diseases.

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LncRNA Rpph1 protects amyloid-β induced neuronal injury in SK-N-SH cells via miR-122/Wnt1 axis

International Journal of Neuroscience ◽

10.1080/00207454.2019.1692834 ◽

2019 ◽

Vol 130 (5) ◽

pp. 443-453 ◽

Cited By ~ 1

Author(s):

Ran Gu ◽

Lu Wang ◽

Man Tang ◽

Shi-Rong Li ◽

Rui Liu ◽

...

Keyword(s):

Amyloid Β ◽

Neuronal Injury

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Mechanical Stretching-Induced Traumatic Brain Injury Is Mediated by the Formation of GSK-3β-Tau Complex to Impair Insulin Signaling Transduction

Biomedicines ◽

10.3390/biomedicines9111650 ◽

2021 ◽

Vol 9 (11) ◽

pp. 1650

Author(s):

Pei-Wen Cheng ◽

Yi-Chung Wu ◽

Tzyy-Yue Wong ◽

Gwo-Ching Sun ◽

Ching-Jiunn Tseng

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Oxidative Dna Damage ◽

Glycogen Synthase ◽

Amyloid Β ◽

Neuronal Injury ◽

Mechanical Injury ◽

Public Health Burden ◽

Increased Risk ◽

Gsk 3Β

Traumatic brain injury confers a significant and growing public health burden. It is a major environmental risk factor for dementia. Nonetheless, the mechanism by which primary mechanical injury leads to neurodegeneration and an increased risk of dementia-related diseases is unclear. Thus, we aimed to investigate the effect of stretching on SH-SY5Y neuroblastoma cells that proliferate in vitro. These cells retain the dopamine-β-hydroxylase activity, thus being suitable for neuromechanistic studies. SH-SY5Y cells were cultured on stretchable membranes. The culture conditions contained two groups, namely non-stretched (control) and stretched. They were subjected to cyclic stretching (6 and 24 h) and 25% elongation at 1 Hz. Following stretching at 25% and 1 Hz for 6 h, the mechanical injury changed the mitochondrial membrane potential and triggered oxidative DNA damage at 24 h. Stretching decreased the level of brain-derived neurotrophic factors and increased amyloid-β, thus indicating neuronal stress. Moreover, the mechanical injury downregulated the insulin pathway and upregulated glycogen synthase kinase 3β (GSK-3β)S9/p-Tau protein levels, which caused a neuronal injury. Following 6 and 24 h of stretching, GSK-3βS9 was directly bound to p-TauS396. In contrast, the neuronal injury was improved using GSK-3β inhibitor TWS119, which downregulated amyloid-β/p-Taus396 phosphorylation by enhancing ERK1/2T202/Y204 and AktS473 phosphorylation. Our findings imply that the neurons were under stress and that the inactivation of the GSK3β could alleviate this defect.

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Additive Microglia-Mediated Neuronal Injury Caused by Amyloid-β and Bacterial TLR Agonists in Murine Neuron-Microglia Co-Cultures Quantified by an Automated Image Analysis using Cognition Network Technology

Journal of Alzheimer s Disease ◽

10.3233/jad-2012-120856 ◽

2012 ◽

Vol 31 (3) ◽

pp. 651-657 ◽

Cited By ~ 10

Author(s):

Sandra Schütze ◽

Tobias Loleit ◽

Moritz Zeretzke ◽

Stephanie Bunkowski ◽

Wolfgang Brück ◽

...

Keyword(s):

Image Analysis ◽

Amyloid Β ◽

Neuronal Injury ◽

Automated Image Analysis ◽

Network Technology ◽

Tlr Agonists

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P1-191: THE ASTROCYTE AUGMENTS THE PRODUCTION OF AMYLOID-β OLIGOMERS LEADING TO NEURONAL INJURY

Alzheimer s & Dementia ◽

10.1016/j.jalz.2018.06.195 ◽

2006 ◽

Vol 14 (7S_Part_6) ◽

pp. P351-P352

Author(s):

Jianping Jia ◽

Wei Wang

Keyword(s):

Amyloid Β ◽

Neuronal Injury

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CircLPAR1/miR-212-3p/ZNF217 feedback loop promotes amyloid β-induced neuronal injury in Alzheimer’s Disease

Brain Research ◽

10.1016/j.brainres.2021.147622 ◽

2021 ◽

pp. 147622

Author(s):

Lifang Wu ◽

Qiang Du ◽

Congcong Wu

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Feedback Loop ◽

Amyloid Β ◽

Neuronal Injury

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The Effect of Anesthesia and Surgery on Postoperative Changes in Plasma biomarkers of neuronal injury, Alzheimer's disease, and inflammation in healthy subjects

10.21203/rs.3.rs-317062/v1 ◽

2021 ◽

Author(s):

Wenguo Fan ◽

Lijia Mai ◽

Zhi Wu ◽

Qiaomei Wu ◽

Xiaoping Yang ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

General Anesthesia ◽

Inflammatory Mediators ◽

Healthy Subjects ◽

Amyloid Β ◽

Neuronal Injury ◽

Increased Risk ◽

Tnf Α ◽

Duration Of Surgery

Abstract Background: Anesthesia and surgery have been linked to neurological sequelae such as perioperative neurocognitive disorders (PND) and increased risk of Alzheimer's disease (AD). The exact mechanisms of PND remain ambiguous and controversial, which were deserved to explore further. Methods: Healthy subjects undergoing general anesthesia for orthognathic surgery were prospectively randomized to receive propofol or sevoflurane for anesthetic maintenance. Blood samples were taken preoperatively and at 3, 24, and 48 hours after surgery. Neurofilament light (NFL), tau, Amyloid β (Aβ)40, Aβ42 and 21 inflammatory mediators in plasma were measured using highly sensitive assays.Results: A total of 50 healthy subjects were enrolled. The mean (SD) age was 24.80(4.63) years. Plasma NFL increased at each measurement from a baseline mean (SD) of 22.3 (20.4) pg/mL to a maximal mean (SD) level of 35.1 (28.7) pg/mL, a maximum increase of 599%, at 3 hours postoperatively. NFL level began to decline at 24 hours, but remained higher at 48 hours. The levels of Aβ40 and Aβ42 decreased at 3 hours, and to minimum mean (SD) of 196.70 (38.61) pg/mL and 8.01(1.66) pg/mL at 24 hours postoperatively, respectively. There were no significant differences in the concentrations of plasma tau after anesthesia and surgery. Plasma IL-6, IL-7, IL-8, IL-10, TNF-α, I-TAC and MIP-1β were significantly increased at 3 hours postoperatively and then declined, which had a similar trajectory with a return to baseline. The peak levels of NFL, IL-6, IL-8, TNF-α and MIP-1β correlated with duration of surgery. The peak plasma NFL level significantly correlated with the levels of IL-6 and IL-8.Conclusions: In the healthy adults, general anesthesia and surgery were associated with an increase in NFL, and a decrease in Aβ40 and Aβ42 in the plasma. Elevated plasma NFL levels might be attributed to many of inflammatory mediators. The data indicate systemic inflammation after anesthesia and surgery may induce neuronal injury. These preliminary findings in healthy subjects could help us to understand the effects of anesthesia/surgery on brain and the potential mechanisms of PND.Trial Registration: The study was registered in Chinese Clinical Trial Registry on Feb 11st, 2019 (ChiCTR1900021289).

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