Restorative effect of endurance exercise on behavioral deficits in the chronic mouse model of Parkinson's disease with severe neurodegeneration

Pothakos, K.; Kurz, Max J.; Lau, Yuen-Sum

doi:10.1186/1471-2202-10-6

Cited by 125 publications

(112 citation statements)

References 46 publications

(53 reference statements)

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“…The challenging beam test is not only useful at detecting motor performance and coordination deficits in genetic mouse models of PD but is also useful in uncovering impairments in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated and 6-hydroxydopamine-treated mice and norepinephrine deficient mice 19,[23][24][25] . In addition, we find the challenging beam to be less influenced by body weight compared to other tests of motor performance and coordination (rotarod and pole test).…”

Section: Discussionmentioning

confidence: 99%

Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease

Fleming

Ekhator

Ghisays

2013

JoVE

130

120

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Sensitive and reliable behavioral outcome measures are essential to the evaluation of potential therapeutic treatments in preclinical trials for many neurodegenerative diseases. In Parkinson's disease, sensorimotor tests sensitive to varying degrees of nigrostriatal dysfunction are fundamental for testing the efficacy of potential therapeutics. Reliable and quite elegant sensorimotor measures exist for rats, however many of these tests measure sensorimotor asymmetry within the rat and are not entirely suitable for the newer genetic mouse models of PD. We have put together a battery of sensorimotor tests inspired by the sensitive tests in rats and adapted for mice. The test battery highlighted in this study is chosen for a) its sensitivity in a wide variety of mouse models of PD, b) its ease in implementing into a study, and c) its low expense. These tests have proven useful in characterizing novel genetic mouse models of PD as well as in testing potential disease-modifying therapies.

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Section: Discussionmentioning

confidence: 99%

Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease

Fleming

Ekhator

Ghisays

2013

JoVE

130

120

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“…The progression of the latter pathological processes is retarded by dietary energy restriction (60) and environmental enrichment (61), and is hastened by diabetes (62). Similarly, dietary energy restriction (63,64) and exercise (65,66) have been reported to delay disease onset and slow progression in mouse models of Parkinson's and Huntington's diseases. A potential advantage of the standard ad libitum laboratory housing conditions is that the disease process is accelerated, and so experimental interventions can be tested more rapidly.…”

Section: Neurological Disordersmentioning

confidence: 99%

“Control” laboratory rodents are metabolically morbid: Why it matters

Martin¹,

Ji²,

Maudsley³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

308

231

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Failure to recognize that many standard control rats and mice used in biomedical research are sedentary, obese, glucose intolerant, and on a trajectory to premature death may confound data interpretation and outcomes of human studies. Fundamental aspects of cellular physiology, vulnerability to oxidative stress, inflammation, and associated diseases are among the many biological processes affected by dietary energy intake and exercise. Although overfed sedentary rodents may be reasonable models for the study of obesity in humans, treatments shown to be efficacious in these animal models may prove ineffective or exhibit novel side effects in active, normalweight subjects.cancer | clinical trials | exercise | insulin resistance | obesity

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“…A selective lesion in the SNpc (Miyoshi et al 2002;Da Cunha et al 2003;Tadaiesky et al 2008), which mainly projects to the striatum, or the systemic MPTP treatment (Pothakos et al 2009) selectively impaired the learning process as well as the memory test performance of rodents in the cued, but not in the spatial, version of MWM. Those behavioral observations were accompanied by a reduction of dopamine levels in the striatum and prefrontal cortex, but not in the hippocampus (Miyoshi et al 2002;Da Cunha et al 2003).…”

Section: -Ohda-and Mptp-based Rodent Modelsmentioning

confidence: 99%

Understanding cognitive deficits in Parkinson’s disease: lessons from preclinical animal models

et al. 2013

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Parkinson's disease (PD) has been, until recently, mainly defined by the presence of characteristic motor symptoms, such as rigidity, tremor, bradykinesia/akinesia, and postural instability. Accordingly, pharmacological and surgical treatments have so far addressed these motor disturbances, leaving nonmotor, cognitive deficits an unmet clinical condition. At the preclinical level, the large majority of studies aiming at defining mechanisms and testing novel therapies have similarly focused on the motor aspects of PD. Unfortunately, deterioration of the executive functions, such as attention, recognition, working memory, and problem solving, often appear in an early, premotor phase of the disease and progressively increase in intensity, negatively affecting the quality of life of 50% -60% of PD patients. At present, the cellular mechanisms underlying cognitive impairments in PD patients are largely unknown and an adequate treatment is still missing. The preclinical research has recently developed new animal models that may open new perspectives for a more integrated approach to the treatment of both motor and cognitive symptoms of the disease. This review will provide an overview on the cognitive symptoms occurring in early PD patients and then focus on the rodent and nonhuman primate models so far available for the study of discriminative and spatial memory attention and learning abilities related to this pathological condition. Cognitive deficits in Parkinson's diseaseParkinson's disease (PD) is a chronic neurodegenerative disorder affecting over four million people worldwide (Dorsey et al. 2007). It is classically characterized by the emergence of motor symptoms such as rigidity, tremor, postural unbalance, and bradykinesia/akinesia (Braak et al. 2003;Jankovic 2008). However, PD also involves nonmotor symptoms (NMS) (Chaudhuri et al. 2006;Jankovic 2008) that appear in the early, often premotor, phase of the disease (Abbott et al. 2005;Abbott 2007;Claassen et al. 2010) and significantly contribute to the impairment of the quality of life of 50%-60% of PD patients (Aarsland et al. 2012). Among others, NMS include olfactory dysfunction, REM sleep disorder, neuropsychiatric disturbances, and cognitive deficits (Schrag et al. 2004;Chaudhuri and Odin 2010). All these symptoms develop independently from each other in the early phase of the disease, and progressively increase in intensity, often leading to dementia in the late phase (Cools et al. 2001;Goetz et al. 2008).Neuropsychiatric mood-related disorders are rather common in PD (Cummings 1992;Schrag et al. 2004) with a prevalence of 20% (Reijnders et al. 2008), and manifest as apathy, depression, and anxiety.On the other hand, cognitive impairments associated with PD are mainly related to the executive functions, resulting in a phenotype resembling that of frontal lobe patients (Robbins and Arnsten 2009), with deficits in attention (Ballard et al. 2002), planning, concept formation, and working memory (Kehagia et al. 2010). In particular, memory deterioration aff...

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Restorative effect of endurance exercise on behavioral deficits in the chronic mouse model of Parkinson's disease with severe neurodegeneration

Cited by 125 publications

References 46 publications

Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease

Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease

“Control” laboratory rodents are metabolically morbid: Why it matters

Understanding cognitive deficits in Parkinson’s disease: lessons from preclinical animal models

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