Molecular Mechanisms Underlying Neuroprotective Effect of Intranasal Administration of Human Hsp70 in Mouse Model of Alzheimer’s Disease

2017 ◽  
Vol 59 (4) ◽  
pp. 1415-1426 ◽  
Author(s):  
Michail B. Evgen’ev ◽  
George S. Krasnov ◽  
Inna V. Nesterova ◽  
David G. Garbuz ◽  
Vadim L. Karpov ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Intranasal Administration ◽  
Molecular Mechanisms ◽  
Neuroprotective Effect ◽  
Model Of Alzheimer’S Disease ◽  
Human Hsp70

scholarly journals Neuroprotective Effects of Tripeptides—Epigenetic Regulators in Mouse Model of Alzheimer’s Disease

2021 ◽  
Vol 14 (6) ◽  
pp. 515
Author(s):  
Vladimir Khavinson ◽  
Anastasiia Ilina ◽  
Nina Kraskovskaya ◽  
Natalia Linkova ◽  
Nina Kolchina ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Dna Sequences ◽  
Dendritic Spine ◽  
Molecular Mechanisms ◽  
Neuroprotective Effect ◽  
Intraperitoneal Administration ◽  
Neuroprotective Effects ◽  
Model Of Alzheimer’S Disease

KED and EDR peptides prevent dendritic spines loss in amyloid synaptotoxicity in in vitro model of Alzheimer’s disease (AD). The objective of this paper was to study epigenetic mechanisms of EDR and KED peptides’ neuroprotective effects on neuroplasticity and dendritic spine morphology in an AD mouse model. Daily intraperitoneal administration of the KED peptide in 5xFAD mice from 2 to 4 months of age at a concentration of 400 μg/kg tended to increase neuroplasticity. KED and EDR peptides prevented dendritic spine loss in 5xFAD-M mice. Their action’s possible molecular mechanisms were investigated by molecular modeling and docking of peptides in dsDNA, containing all possible combinations of hexanucleotide sequences. Similar DNA sequences were found in the lowest-energy complexes of the studied peptides with DNA in the classical B-form. EDR peptide has binding sites in the promoter region of CASP3, NES, GAP43, APOE, SOD2, PPARA, PPARG, GDX1 genes. Protein products of these genes are involved in AD pathogenesis. The neuroprotective effect of EDR and KED peptides in AD can be defined by their ability to prevent dendritic spine elimination and neuroplasticity impairments at the molecular epigenetic level.

scholarly journals Neuroprotective Effect of Caffeic Acid Phenethyl Ester in A Mouse Model of Alzheimer’s Disease Involves Nrf2/HO-1 Pathway

2018 ◽  
Vol 9 (4) ◽  
pp. 605 ◽  
Author(s):  
Fabiana Morroni ◽  
Giulia Sita ◽  
Agnese Graziosi ◽  
Eleonora Turrini ◽  
Carmela Fimognari ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Caffeic Acid ◽  
Neuroprotective Effect ◽  
Caffeic Acid Phenethyl Ester ◽  
Model Of Alzheimer’S Disease

The Effect of Human HSP70 Administration on a Mouse Model of Alzheimer’s Disease Strongly Depends on Transgenicity and Age

2019 ◽  
Vol 67 (4) ◽  
pp. 1391-1404 ◽  
Author(s):  
Michael Evgen’ev ◽  
Natalia Bobkova ◽  
George Krasnov ◽  
David Garbuz ◽  
Sergei Funikov ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Human Hsp70

scholarly journals Repetitive transcranial magnetic stimulation increases the brain’s drainage efficiency in a mouse model of Alzheimer’s disease

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Yangyang Lin ◽  
Jian Jin ◽  
Rongke Lv ◽  
Yuan Luo ◽  
Weiping Dai ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transcranial Magnetic Stimulation ◽  
Mouse Model ◽  
Magnetic Stimulation ◽  
Molecular Mechanisms ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Model Of Alzheimer’S Disease ◽  
5Xfad Mouse ◽  
5Xfad Mice

AbstractAlzheimer’s disease (AD) is a progressive neurodegenerative disease with high prevalence rate among the elderly population. A large number of clinical studies have suggested repetitive transcranial magnetic stimulation (rTMS) as a promising non-invasive treatment for patients with mild to moderate AD. However, the underlying cellular and molecular mechanisms remain largely uninvestigated. In the current study, we examined the effect of high frequency rTMS treatment on the cognitive functions and pathological changes in the brains of 4- to 5-month old 5xFAD mice, an early pathological stage with pronounced amyloidopathy and cognitive deficit. Our results showed that rTMS treatment effectively prevented the decline of long-term memories of the 5xFAD mice for novel objects and locations. Importantly, rTMS treatment significantly increased the drainage efficiency of brain clearance pathways, including the glymphatic system in brain parenchyma and the meningeal lymphatics, in the 5xFAD mouse model. Significant reduction of Aβ deposits, suppression of microglia and astrocyte activation, and prevention of decline of neuronal activity as indicated by the elevated c-FOS expression, were observed in the prefrontal cortex and hippocampus of the rTMS-treated 5xFAD mice. Collectively, these findings provide a novel mechanistic insight of rTMS in regulating brain drainage system and β-amyloid clearance in the 5xFAD mouse model, and suggest the potential use of the clearance rate of contrast tracer in cerebrospinal fluid as a prognostic biomarker for the effectiveness of rTMS treatment in AD patients.

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