Investigation of the protective effect of long-term exercise on molecular pathways and behaviours in scopolamine induced alzheimer's disease-like condition

Köse, Seda; Kutlu, Meltem Dönmez; Kara, Samet; Polat, Sait; Akıllıoğlu, Kübra

doi:10.1016/j.brainres.2023.148429

Cited by 5 publications

(2 citation statements)

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“…administration of scopolamine in mice and rats induces cholinergic dysfunction and increase of AChE that further cleaves acetylcholine at the synapses leading to amnesia and cognitive loss. Doses administered range from 0.4 mg/kg to 3 mg/kg i.p., with longer-lasting memory impairment after repeated daily administration for one or more weeks than a single injection ( Rahimzadegan and Soodi, 2018 ; Chen and Yeong, 2020 ; Kose et al, 2023 ). This model is mainly used for behavioral studies, but some authors report that scopolamine induces an imbalance of the amyloid-beta precursor protein (APP) processing to the amyloidogenic pathway causing intraneuronal accumulation of amyloid-beta (Aß) and also increased tau synthesis ( Chen and Yeong, 2020 ; Kose et al, 2023 ).…”

Section: Validated and New Experimental Models Of Neurodegenerationmentioning

confidence: 99%

“…Doses administered range from 0.4 mg/kg to 3 mg/kg i.p., with longer-lasting memory impairment after repeated daily administration for one or more weeks than a single injection ( Rahimzadegan and Soodi, 2018 ; Chen and Yeong, 2020 ; Kose et al, 2023 ). This model is mainly used for behavioral studies, but some authors report that scopolamine induces an imbalance of the amyloid-beta precursor protein (APP) processing to the amyloidogenic pathway causing intraneuronal accumulation of amyloid-beta (Aß) and also increased tau synthesis ( Chen and Yeong, 2020 ; Kose et al, 2023 ). Noticeably, the scopolamine model in mice and, to a minor extent, in rats, was found the most widely used in vivo model for multitarget anti-AD drug discovery in a bibliometric analysis of the last 3 decades ( Sampietro et al, 2022 ).…”

Section: Validated and New Experimental Models Of Neurodegenerationmentioning

confidence: 99%

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New insights in animal models of neurotoxicity-induced neurodegeneration

Sanfeliu,

Bartra,

Suñol

et al. 2024

Front. Neurosci.

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The high prevalence of neurodegenerative diseases is an unintended consequence of the high longevity of the population, together with the lack of effective preventive and therapeutic options. There is great pressure on preclinical research, and both old and new models of neurodegenerative diseases are required to increase the pipeline of new drugs for clinical testing. We review here the main models of neurotoxicity-based animal models leading to central neurodegeneration. Our main focus was on studying how changes in neurotransmission and neuroinflammation, mainly in rodent models, contribute to harmful processes linked to neurodegeneration. The majority of the models currently in use mimic Parkinson’s disease (PD) and Alzheimer’s disease (AD), which are the most common neurodegenerative conditions in older adults. AD is the most common age-related dementia, whereas PD is the most common movement disorder with also cases of dementia. Several natural toxins and xenobiotic agents induce dopaminergic neurodegeneration and can reproduce neuropathological traits of PD. The literature analysis of MPTP, 6-OH-dopamine, and rotenone models suggested the latter as a useful model when specific doses of rotenone were administrated systemically to C57BL/6 mice. Cholinergic neurodegeneration is mainly modelled with the toxin scopolamine, which is a useful rodent model for the screening of protective drugs against cognitive decline and AD. Several agents have been used to model neuroinflammation-based neurodegeneration and dementia in AD, including lipopolysaccharide (LPS), streptozotocin, and monomeric C-reactive protein. The bacterial agent LPS makes a useful rodent model for testing anti-inflammatory therapies to halt the development and severity of AD. However, neurotoxin models might be more useful than genetic models for drug discovery in PD but that is not the case in AD where they cannot beat the new developments in transgenic mouse models. Overall, we should work using all available models, either in vivo, in vitro, or in silico, considering the seriousness of the moment and urgency of developing effective drugs.

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