Maintained memory and long‐term potentiation in a mouse model of Alzheimer's disease with both amyloid pathology and human tau

Netsyk, Olga; Pickett, Eleanor; Herrmann, Abigail G.; Jain, Pooja; Stevenson, Anna J.; Oren, Iris; Hardt, Oliver; Spires‐Jones, Tara L.

doi:10.1111/ejn.14918

Cited by 5 publications

(4 citation statements)

References 39 publications

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“…Due to an age-dependent memory decline in this task at 9month-old, no genotype or prior training effects are detected. It is likely that stronger training is needed for revealing the long-term recognition memory [87]. The same sampling duration that enables object recognition memory is insufficient for forming and/or retaining object location memory.…”

Section: Intact Working Memory and Recognition In App/ps1 Mice 25mentioning

confidence: 99%

Mid-Adulthood Cognitive Training Improves Performance in a Spatial Task but Does Not Ameliorate Hippocampal Pathology in a Mouse Model of Alzheimer’s Disease

Williams

Mutlu-Smith

Alex

et al. 2023

JAD

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Background: Prior experience in early life has been shown to improve performance in aging and mice with Alzheimer’s disease (AD) pathology. However, whether cognitive training at a later life stage would benefit subsequent cognition and reduce pathology in AD mice needs to be better understood. Objective: This study aimed to verify if behavioral training in mid-adulthood would improve subsequent cognition and reduce AD pathology and astrogliosis. Methods: Mixed-sex APP/PS1 and wildtype littermate mice received a battery of behavioral training, composed of spontaneous alternation in the Y-maze, novel object recognition and location tasks, and spatial training in the water maze, or handling only at 7 months of age. The impact of AD genotype and prior training on subsequent learning and memory of aforementioned tasks were assessed at 9 months. Results: APP/PS1 mice made more errors than wildtype littermates in the radial-arm water maze (RAWM) task. Prior training prevented this impairment in APP/PS1 mice. Prior training also contributed to better efficiency in finding the escape platform in both APP/PS1 mice and wildtype littermates. Short-term and long-term memory of this RAWM task, of a reversal task, and of a transfer task were comparable among APP/PS1 and wildtype mice, with or without prior training. Amyloid pathology and astrogliosis in the hippocampus were also comparable between the APP/PS1 groups. Conclusion: These data suggest that cognitive training in mid-adulthood improves subsequent accuracy in AD mice and efficiency in all mice in the spatial task. Cognitive training in mid-adulthood provides no clear benefit on memory or on amyloid pathology in midlife.

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Section: Intact Working Memory and Recognition In App/ps1 Mice 25mentioning

confidence: 99%

Mid-Adulthood Cognitive Training Improves Performance in a Spatial Task but Does Not Ameliorate Hippocampal Pathology in a Mouse Model of Alzheimer’s Disease

Williams

Mutlu-Smith

Alex

et al. 2023

JAD

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“…This observation is confirmed by PET scanning of amyloids, which highlights deposition in various brain regions [122]. Several mechanisms have been suggested to contribute to the neurodegeneration induced by amyloid toxicity, including mitochondrial dysfunction with Ca 2+ release and oxidative stress [123,124], ion channel pore formation in neuronal membranes [125], loss of hippocampal long-term potentiation with memory and learning impairment [126], neuronal hyperactivation by the suppression of glutamate reuptake [127,128], and receptor binding (e.g., cellular prion protein, receptor for advanced glycation endproducts RAGE, p75 neurotrophin receptor p75NTR, neurexin1 NgR1, ephrin-B2 EphB2, and FcγRIIb receptor) [129].…”

Section: Ad Biomarkersmentioning

confidence: 59%

Retinal Alterations Predict Early Prodromal Signs of Neurodegenerative Disease

Casciano,

Zauli,

Celeghini

et al. 2024

IJMS

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Neurodegenerative diseases are an increasingly common group of diseases that occur late in life with a significant impact on personal, family, and economic life. Among these, Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the major disorders that lead to mild to severe cognitive and physical impairment and dementia. Interestingly, those diseases may show onset of prodromal symptoms early after middle age. Commonly, the evaluation of these neurodegenerative diseases is based on the detection of biomarkers, where functional and structural magnetic resonance imaging (MRI) have shown a central role in revealing early or prodromal phases, although it can be expensive, time-consuming, and not always available. The aforementioned diseases have a common impact on the visual system due to the pathophysiological mechanisms shared between the eye and the brain. In Parkinson’s disease, α-synuclein deposition in the retinal cells, as well as in dopaminergic neurons of the substantia nigra, alters the visual cortex and retinal function, resulting in modifications to the visual field. Similarly, the visual cortex is modified by the neurofibrillary tangles and neuritic amyloid β plaques typically seen in the Alzheimer’s disease brain, and this may reflect the accumulation of these biomarkers in the retina during the early stages of the disease, as seen in postmortem retinas of AD patients. In this light, the ophthalmic evaluation of retinal neurodegeneration could become a cost-effective method for the early diagnosis of those diseases, overcoming the limitations of functional and structural imaging of the deep brain. This analysis is commonly used in ophthalmic practice, and interest in it has risen in recent years. This review will discuss the relationship between Alzheimer’s disease and Parkinson’s disease with retinal degeneration, highlighting how retinal analysis may represent a noninvasive and straightforward method for the early diagnosis of these neurodegenerative diseases.

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“…In this study, we found that the MAPK pathway and neurotrophin signaling pathway were involved in the biological regulation of HDAC1 and HDAC8 with AD. All these pathways played a prominent role in AD pathology [ [36] , [37] , [38] , [39] , [40] ]. Our study provided a new therapy discovery on the impact of HDAC1 and HDAC8 involved in the neuropathology and genesis of AD and provided a supportive proof how HDAC8 participated in AD disease progression.…”

Section: Discussionmentioning

confidence: 99%

Transcriptome analysis identifies the role of Class I histone deacetylase in Alzheimer’s disease

Geng,

Zhao,

Chen

et al. 2023

Heliyon

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Maintained memory and long‐term potentiation in a mouse model of Alzheimer's disease with both amyloid pathology and human tau

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 5 publications

References 39 publications

Mid-Adulthood Cognitive Training Improves Performance in a Spatial Task but Does Not Ameliorate Hippocampal Pathology in a Mouse Model of Alzheimer’s Disease

Mid-Adulthood Cognitive Training Improves Performance in a Spatial Task but Does Not Ameliorate Hippocampal Pathology in a Mouse Model of Alzheimer’s Disease

Retinal Alterations Predict Early Prodromal Signs of Neurodegenerative Disease

Transcriptome analysis identifies the role of Class I histone deacetylase in Alzheimer’s disease

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