NeuroScale, the battery of behavioral tests with novel scoring system for phenotyping of transgenic rat model of tauopathy

Korenova, Miroslava; Žilka, Norbert; Stozicka, Zuzana; Bugos, Ondrej; Vanický, Ivo; Novák, Michal

doi:10.1016/j.jneumeth.2008.09.027

Cited by 33 publications

(27 citation statements)

References 33 publications

(43 reference statements)

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“…Because of the bigger size of rats, the ledge test was performed on a thin beam (width, 1 cm) instead of the cage ledge. The scoring was performed as described (Guyenet et al, 2010).…”

Section: Behavioral Testsmentioning

confidence: 99%

“…To assess progression of disease severity in TBPQ64 rats over time, we first repeatedly applied a modified ataxia score test (Guyenet et al, 2010), which has been successfully used in mouse models of cerebellar ataxia type 7. As expected, with increasing age the ataxia score increased significantly in SCA17 rats, reflecting a progression of symptoms ( Fig.…”

Section: Motor Deficits and Increased Anxiety In Sca17 Ratsmentioning

confidence: 99%

“…Since psychiatric symptoms and behavioral symptoms are present in SCA17 patients, we assessed anxiety in the EPM test, which has been validated behaviorally and pharmacologically extensively (Pellow et al, 1985;Huang et al, 2012). Already at the age of 4 months, significant differences were found between TBPQ64 rats and their wild-type littermates (Fig.…”

Section: Motor Deficits and Increased Anxiety In Sca17 Ratsmentioning

confidence: 99%

“…Although two transgenic mouse models (Friedman et al, 2007;Chang et al, 2011) and one knock-in mouse model (Huang et al, 2011) already exist, which all mimic several phenotypic characteristics of the disease, mouse models are in general limited for studying certain functional and behavioral measurements (Tecott and Nestler, 2004;Rodriguiz and Wetsel, 2006;Herrmann et al, 2012). Rats, on the other hand, show excellent learning abilities compared to mice and are the species of choice for studying learning and memory in rodents and for pharmacological manipulations (Kujpers, 1999).…”

Section: Introductionmentioning

confidence: 99%

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A Novel Transgenic Rat Model for Spinocerebellar Ataxia Type 17 Recapitulates Neuropathological Changes and SuppliesIn VivoImaging Biomarkers

Kelp

Koeppen²,

Petrasch‐Parwez

et al. 2013

J. Neurosci.

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Spinocerebellar ataxia 17 (SCA17) is an autosomal-dominant, late-onset neurodegenerative disorder caused by an expanded polyglutamine (polyQ) repeat in the TATA-box-binding protein (TBP). To further investigate this devastating disease, we sought to create a first transgenic rat model for SCA17 that carries a full human cDNA fragment of the TBP gene with 64 CAA/CAG repeats (TBPQ64). In line with previous observations in mouse models for SCA17, TBPQ64 rats show a severe neurological phenotype including ataxia, impairment of postural reflexes, and hyperactivity in early stages followed by reduced activity, loss of body weight, and early death. Neuropathologically, the severe phenotype of SCA17 rats was associated with neuronal loss, particularly in the cerebellum. Degeneration of Purkinje, basket, and stellate cells, changes in the morphology of the dendrites, nuclear TBP-positive immunoreactivity, and axonal torpedos were readily found by light and electron microscopy. While some of these changes are well recapitulated in existing mouse models for SCA17, we provide evidence that some crucial characteristics of SCA17 are better mirrored in TBPQ64 rats. Thus, this SCA17 model represents a valuable tool to pursue experimentation and therapeutic approaches that may be difficult or impossible to perform with SCA17 transgenic mice. We show for the first time positron emission tomography (PET) and diffusion tensor imaging (DTI) data of a SCA animal model that replicate recent PET studies in human SCA17 patients. Our results also confirm that DTI are potentially useful correlates of neuropathological changes in TBPQ64 rats and raise hope that DTI imaging could provide a biomarker for SCA17 patients.

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“…Because of the bigger size of rats, the ledge test was performed on a thin beam (width, 1 cm) instead of the cage ledge. The scoring was performed as described (Guyenet et al, 2010).…”

Section: Behavioral Testsmentioning

confidence: 99%

Section: Motor Deficits and Increased Anxiety In Sca17 Ratsmentioning

confidence: 99%

Section: Motor Deficits and Increased Anxiety In Sca17 Ratsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

A Novel Transgenic Rat Model for Spinocerebellar Ataxia Type 17 Recapitulates Neuropathological Changes and SuppliesIn VivoImaging Biomarkers

Kelp

Koeppen²,

Petrasch‐Parwez

et al. 2013

J. Neurosci.

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show abstract

“…Standardization of behavioural or neuropathological readouts do not exist, also there is no grading system as is usual for human patients. First recommendations for phenotyping strategies of mice (Crawley 2008) and of a scoring system to phenotype transgenic rats (Korenova et al 2009) have been made without general agreement on which terms to use.…”

Section: Olaf Riessmentioning

confidence: 99%

1st INCF Workshop on Genetic Animal Models for Brain Diseases

Rieß¹,

Graeßner²

2011

Nature Precedings

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A comparative study on pathological features of transgenic rat lines expressing either three or four repeat misfolded tau

Valachova

Brezováková

Bugos

et al. 2018

J of Comparative Neurology

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Human tauopathies represent a heterogeneous group of neurodegenerative disorders characterized by distinct clinical features, typical histopathological structures, and defined ratio(s) of three-repeat and four-repeat tau isoforms within pathological aggregates. How the optional microtubule-binding repeat of tau influences this differentiation of pathologies is understudied. We have previously generated and characterized transgenic rodent models expressing human truncated tau aa151-391 with either three (SHR24) or four microtubule-binding repeats (SHR72). Here, we compare the behavioral and neuropathological hallmarks of these two transgenic lines using a battery of tests for sensorimotor, cognitive, and neurological functions over the age range of 3.5-15 months. Progression of sensorimotor and neurological deficits was similar in both transgenic lines; however, the lifespan of transgenic line SHR72 expressing truncated four-repeat tau was markedly shorter than SHR24. Moreover, the expression of three or four-repeat tau induced distinct neurofibrillary pathology in these lines. Transgenic lines displayed different distribution of tau pathology and different type of neurofibrillary tangles. Our results suggest that three- and four-repeat isoforms of tau may display different modes of action in the diseased brain.

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NeuroScale, the battery of behavioral tests with novel scoring system for phenotyping of transgenic rat model of tauopathy

Cited by 33 publications

References 33 publications

A Novel Transgenic Rat Model for Spinocerebellar Ataxia Type 17 Recapitulates Neuropathological Changes and SuppliesIn VivoImaging Biomarkers

A Novel Transgenic Rat Model for Spinocerebellar Ataxia Type 17 Recapitulates Neuropathological Changes and SuppliesIn VivoImaging Biomarkers

1st INCF Workshop on Genetic Animal Models for Brain Diseases

A comparative study on pathological features of transgenic rat lines expressing either three or four repeat misfolded tau

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