Role of F3/contactin expression profile in synaptic plasticity and memory in aged mice

Puzzo, Daniela; Bizzoca, Antonella; Loreto, Carla; Guida, Chiara; Gulisano, Walter; Frasca, Giampiero; Bellomo, Maria; Castorina, Sergio; Gennarini, Gianfranco; Palmeri, Agostino

doi:10.1016/j.neurobiolaging.2015.01.004

Cited by 29 publications

(21 citation statements)

References 129 publications

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“…However, even in this selected subgroup with increased levels of inflammatory and oxidative stress markers, no correlation between altered behaviour and specific neuropathological symptoms could be established [50]. The stated impairments of spatial memory and cognition in aged degus [14] may therefore be just a part of the normal aging process, since physiologic aging is linked to significant impairments in memory [51], cognition [52] and hippocampal long-term potentiation [53] in mice as well. Thus, symptoms of normal aging may not be misinterpreted to model AD.…”

Section: Discussionmentioning

confidence: 99%

Revisiting rodent models: Octodon degus as Alzheimer’s disease model?

Steffen

Krohn

Paarmann

et al. 2016

acta neuropathol commun

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Alzheimer’s disease primarily occurs as sporadic disease and is accompanied with vast socio-economic problems. The mandatory basic research relies on robust and reliable disease models to overcome increasing incidence and emerging social challenges. Rodent models are most efficient, versatile, and predominantly used in research. However, only highly artificial and mostly genetically modified models are available. As these ‘engineered’ models reproduce only isolated features, researchers demand more suitable models of sporadic neurodegenerative diseases. One very promising animal model was the South American rodent Octodon degus, which was repeatedly described as natural ‘sporadic Alzheimer’s disease model’ with ‘Alzheimer’s disease-like neuropathology’. To unveil advantages over the ‘artificial’ mouse models, we re-evaluated the age-dependent, neurohistological changes in young and aged Octodon degus (1 to 5-years-old) bred in a wild-type colony in Germany. In our hands, extensive neuropathological analyses of young and aged animals revealed normal age-related cortical changes without obvious signs for extensive degeneration as seen in patients with dementia. Neither significant neuronal loss nor enhanced microglial activation were observed in aged animals. Silver impregnation methods, conventional, and immunohistological stains as well as biochemical fractionations revealed neither amyloid accumulation nor tangle formation. Phosphoepitope-specific antibodies against tau species displayed similar intraneuronal reactivity in both, young and aged Octodon degus.In contrast to previous results, our study suggests that Octodon degus born and bred in captivity do not inevitably develop cortical amyloidosis, tangle formation or neuronal loss as seen in Alzheimer’s disease patients or transgenic disease models.

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Section: Discussionmentioning

confidence: 99%

Revisiting rodent models: Octodon degus as Alzheimer’s disease model?

Steffen

Krohn

Paarmann

et al. 2016

acta neuropathol commun

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“…Recently, we have also used animal models of aging [77–79]. In this case, notwithstanding genetically- or drug-induced animal models of aging were available [80–83], we preferred to use a physiological model of aging to provide more realistic information on the natural development of the aging process.…”

Section: Non-transgenic Models For the Study Of Admentioning

confidence: 99%

Rodent models for Alzheimer’s disease drug discovery

Puzzo

Gulisano

Palmeri

et al. 2015

Expert Opinion on Drug Discovery

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113

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Introduction Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by memory loss and personality changes, leading to dementia. Histophatological hallmarks are represented by aggregates of beta-amyloid peptide (Aβ) in senile plaques and deposition of hyperphosphorylated tau protein in neurofibrillary tangles in the brain. Rare forms of early onset familial Alzheimer's disease are due to gene mutations. This has prompted researchers to develop genetically modified animals that could recapitulate the main features of the disease. The use of these models is complemented by non-genetically modified animals. Area covered This review summarizes the characteristics of the most used transgenic (Tg) and non-Tg models of AD. The authors have focused on models mainly used in their laboratories including: APP Tg2576, APP/PS1, 3xAD, single h-Tau, non-Tg mice treated with acute injections of Aβ or tau, and models of physiological aging. Expert opinion Animal models of disease might be very useful for studying the pathophysiology of the disease and for testing new therapeutics in preclinical studies but they do not reproduce the entire clinical features of human AD. When selecting a model, researchers should consider the various factors that might influence the phenotype. They should also consider the timing of testing/treating animals since the age at which each model develops certain aspects of the AD pathology varies.

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“…Therefore, it is important to understand the alterations in physiological parameters and synaptic plasticity that occur during normal healthy aging, not just in neurodegenerative conditions. A number of previous studies have demonstrated that synaptic plasticity significantly decreases with increasing age in healthy animals (13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Age-associated alterations in constitutively expressed cyclooxygenase-2 immunoreactivity and protein levels in the hippocampus

Jung

Yoo

Kim

et al. 2017

Molecular Medicine Reports

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Abstract. Cyclooxygenase-2 (COX-2) is a known inducible inflammatory mediator. COX-2 is constitutively expressed in the hippocampus and may regulate synaptic plasticity. The present study investigated the age-associated alterations in white blood cell counts and hippocampal COX-2 expression in healthy mice using immunohistochemical and western blot analyses at 1 month postnatal (PM1), PM3, PM6, PM12 and PM24. White blood cell counts were significantly decreased in the PM24 group when compared with the PM1 group. In addition, lymphocyte counts were decreased in the PM24 group when compared with all other groups. By contrast, monocyte, neutrophil and eosinophil counts were increased in the PM24 group; however, this did not reach statistical significance. COX-2 expression was identified in the granule cells of the dentate gyrus and in the pyramidal cells of the hippocampal CA2/3 region. COX-2 immunoreactivity was maintained until PM18, however, the levels significantly decreased by PM24. These results suggest that, despite alterations in the differential white blood cell counts, the significant decrease in constitutive COX-2 expression in the hippocampus may be associated with degenerative age-associated alterations in synaptic plasticity in the hippocampus.

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Role of F3/contactin expression profile in synaptic plasticity and memory in aged mice

Cited by 29 publications

References 129 publications

Revisiting rodent models: Octodon degus as Alzheimer’s disease model?

Revisiting rodent models: Octodon degus as Alzheimer’s disease model?

Rodent models for Alzheimer’s disease drug discovery

Age-associated alterations in constitutively expressed cyclooxygenase-2 immunoreactivity and protein levels in the hippocampus

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