scholarly journals APOE genotype and sex influence memory and dendritic spine density in an EFAD mouse model of Alzheimer’s disease

2020 ◽  
Vol 16 (S3) ◽  
Author(s):  
Lisa R Taxier ◽  
Sarah M Philippi ◽  
Jason York ◽  
Mary Jo LaDu ◽  
Karyn M Frick
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Dendritic Spine ◽  
Apoe Genotype ◽  
Spine Density ◽  
Sex Influence ◽  
Dendritic Spine Density ◽  
Model Of Alzheimer’S Disease

scholarly journals Early Activation of Experience-Independent Dendritic Spine Turnover in a Mouse Model of Alzheimer's Disease

2016 ◽  
Author(s):  
Jacqueline K. Heiss ◽  
Joshua Barrett ◽  
Zizi Yu ◽  
Laura T. Haas ◽  
Mikhail A. Kostylev ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Dendritic Spine ◽  
Early Activation ◽  
Model Of Alzheimer’S Disease

scholarly journals EphA4 loss improves social memory performance and alters dendritic spine morphology without changes in amyloid pathology in a mouse model of Alzheimer’s disease

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Lindsay Poppe ◽  
Laura Rué ◽  
Mieke Timmers ◽  
Annette Lenaerts ◽  
Annet Storm ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Dendritic Spine ◽  
Cognitive Functions ◽  
Social Memory ◽  
Beta Amyloid ◽  
Amyloid Peptide ◽  
Spine Morphology ◽  
Model Of Alzheimer’S Disease

Abstract Background EphA4 is a receptor of the ephrin system regulating spine morphology and plasticity in the brain. These processes are pivotal in the pathophysiology of Alzheimer’s disease (AD), characterized by synapse dysfunction and loss, and the progressive loss of memory and other cognitive functions. Reduced EphA4 signaling has been shown to rescue beta-amyloid-induced dendritic spine loss and long-term potentiation (LTP) deficits in cultured hippocampal slices and primary hippocampal cultures. In this study, we investigated whether EphA4 ablation might preserve synapse function and ameliorate cognitive performance in the APPPS1 transgenic mouse model of AD. Methods A postnatal genetic ablation of EphA4 in the forebrain was established in the APPPS1 mouse model of AD, followed by a battery of cognitive tests at 9 months of age to investigate cognitive function upon EphA4 loss. A Golgi-Cox staining was used to explore alterations in dendritic spine density and morphology in the CA1 region of the hippocampus. Results Upon EphA4 loss in APPPS1 mice, we observed improved social memory in the preference for social novelty test without affecting other cognitive functions. Dendritic spine analysis revealed altered synapse morphology as characterized by increased dendritic spine length and head width. These modifications were independent of hippocampal plaque load and beta-amyloid peptide levels since these were similar in mice with normal versus reduced levels of EphA4. Conclusion Loss of EphA4 improved social memory in a mouse model of Alzheimer’s disease in association with alterations in spine morphology.

scholarly journals APOE genotype, sex, and ovariectomy influence anxiety‐like behaviors in an EFAD mouse model of Alzheimer’s disease

2020 ◽  
Vol 16 (S3) ◽  
Author(s):  
Sarah M Philippi ◽  
Lisa R Taxier ◽  
Jason York ◽  
Mary Jo LaDu ◽  
Karyn M Frick
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Apoe Genotype ◽  
Model Of Alzheimer’S Disease

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.

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