Pharmacokinetics of [18F]flutemetamol in wild-type rodents and its binding to beta amyloid deposits in a mouse model of Alzheimer’s disease

2012 ◽  
Vol 39 (11) ◽  
pp. 1784-1795 ◽  
Author(s):  
Anniina Snellman ◽  
Johanna Rokka ◽  
Francisco R. Lopez-Picon ◽  
Olli Eskola ◽  
Ian Wilson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Beta Amyloid ◽  
Wild Type ◽  
Model Of Alzheimer’S Disease ◽  
Amyloid Deposits

TSPO and amyloid deposits in sub-regions of the hippocampus in the 3xTgAD mouse model of Alzheimer’s disease

2019 ◽  
Vol 121 ◽  
pp. 95-105 ◽  
Author(s):  
Benjamin B. Tournier ◽  
Stergios Tsartsalis ◽  
Daphney Rigaud ◽  
Christine Fossey ◽  
Thomas Cailly ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Amyloid Deposits

β-Lapachone attenuates cognitive impairment and neuroinflammation in beta-amyloid induced mouse model of Alzheimer's disease

2020 ◽  
Vol 81 ◽  
pp. 106300 ◽  
Author(s):  
Narmin Mokarizadeh ◽  
Pouran Karimi ◽  
Marjan Erfani ◽  
Saeed Sadigh-Eteghad ◽  
Nazila Fathi Maroufi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mouse Model ◽  
Beta Amyloid ◽  
Model Of Alzheimer’S Disease

Selenomethionine reduces the deposition of beta-amyloid plaques by modulating β-secretase and enhancing selenoenzymatic activity in a mouse model of Alzheimer's disease

Metallomics ◽  
2016 ◽  
Vol 8 (8) ◽  
pp. 782-789 ◽  
Author(s):  
Zhong-Hao Zhang ◽  
Chen Chen ◽  
Qiu-Yan Wu ◽  
Rui Zheng ◽  
Qiong Liu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Plaques ◽  
Beta Amyloid ◽  
Model Of Alzheimer’S Disease ◽  
Aβ Production

Effects on Aβ production and the probable connection among selenoenzymes, GSK3β and Aβ pathology by selenomethionine treatment in AD mice.

P2-381: Tg4-42: A new mouse model of Alzheimer's disease-N-truncated beta-amyloid 4-42 affects memory decline and synaptic plasticity

2013 ◽  
Vol 9 ◽  
pp. P498-P498 ◽  
Author(s):  
Katharina Dietrich ◽  
Yvonne Bouter ◽  
Jessica Wittnam ◽  
Thierry Pillot ◽  
Sophie Papot-Couturier ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Mouse Model ◽  
Beta Amyloid ◽  
Memory Decline ◽  
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.

Effect of Soluble Amyloid Precursor Protein-alpha on Adult Hippocampal Neurogenesis in a Mouse Model of Alzheimer’s Disease

2021 ◽  
Author(s):  
Shane M. Ohline ◽  
Connie Chan ◽  
Lucia Schoderboeck ◽  
Hollie E. Wicky ◽  
Warren P. Tate ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Precursor Protein ◽  
Hippocampal Neurogenesis ◽  
Precursor Protein ◽  
Adult Hippocampal Neurogenesis ◽  
Wild Type ◽  
Viral Expression ◽  
Model Of Alzheimer’S Disease

Abstract Soluble amyloid precursor protein-alpha (sAPPα) is a regulator of neuronal and memory mechanisms, while also having neurogenic and neuroprotective effects in the brain. As adult hippocampal neurogenesis is impaired in Alzheimer’s disease, we tested the hypothesis that sAPPα delivery would rescue adult hippocampal neurogenesis in an APP/PS1 mouse model of Alzheimer’s disease. An adeno-associated virus-9 (AAV9) encoding murine sAPPα was injected into the hippocampus of 8 month-old wild-type and APP/PS1 mice, and later two different thymidine analogues (XdU) were systemically injected to label adult-born cells at different time points after viral transduction. The proliferation of adult-born cells, cell survival after eight weeks, and cell differentiation into either neurons or astrocytes was studied. Proliferation was impaired in APP/PS1 mice but was restored to wild-type levels by viral expression of sAPPα. In contrast, sAPPα overexpression failed to rescue the survival of XdU+-labelled cells that was impaired in APP/PS1 mice, although it did cause a significant increase in the area density of astrocytes in the granule cell layer across both genotypes. Finally, viral expression of sAPPα reduced amyloid-beta plaque load in APP/PS1 mice in the dentate gyrus and somatosensory cortex. These data add further evidence that increased levels of sAPPα could be therapeutic for the cognitive decline in AD, in part through restoration of the proliferation of neural progenitor cells in adults.

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