MTR and In-vivo 1H-MRS studies on mouse brain with parkinson’s disease

Yoon, Moon-Hyun; Kim, Hyeon Jin; Chung, Jin Yeung; Doo, Ah Reum; Park, Hi-Joon; Kim, Seung Nam; Choe, Bo-Young

doi:10.3938/jkps.61.1852

Cited by 1 publication

(1 citation statement)

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“…Other forms of neurodegenerative diseases which are caused by misfolded proteins include Parkinson’s (PD) and Huntington’s disease (HD). In PD mice, the MTR was significantly decreased in the striatum and substantia nigra and it was significantly associated with an increase in the Glu/Cr ratio compared with the control group (28). Additionally, a tendency towards a reduction in T 2 was measured in the model animals as compared to littermates (29).…”

Section: Discussionmentioning

confidence: 99%

Mapping prion pathology in mice using quantitative imaging: an MRI study

Demetriou

Tachrount

Ellis

et al. 2021

Preprint

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Human prion diseases are fatal neurodegenerative disorders which cause cognitive impairment and neurological deficits. Additional measures of tissue status are necessary for improving the sensitivity and specificity of clinical diagnosis as in many cases clinical forms of prion disease are commonly mistaken for other forms of dementia. To that effect, we developed a set of quantitative magnetic resonance-based tools, including magnetic resonance spectroscopy (MRS), magnetization transfer ratio (MTR) and quantitative T1 and T2 imaging to study the course of the disease in an animal model of prion disease. Using in vivo MTR, significant changes were detected in the cortex and thalamus of late-stage prion -infected mice as compared to littermates. In addition, we found a significant increase of MTR in thalamus and cortex of 80 dpi healthy mice when compared with 160 dpi healthy mice suggestive of changes occurring during the development of the brain. Using quantitative T2 mapping, significantly higher values were measured in thalamus of prion mice at all stages of the disease (T2=40ms) while T1 was found to be significantly higher in cortex (T1=1.89s) and hippocampus, albeit only in late-stage prion mice as compared to aged-matched controls (T1=1.67s). Using quantitative MRS significant changes were detected in glutamate (Glu) and myo-inositol (Ins) at all stages of prion disease when compared with the control group. NAA, Cr, Lactate and Lipids were only found to be significantly different at early and late stages of the disease while Taurine (Tau) was only significantly increased in the asymptomatic stage without any significant change at early and late stages of the disease. These changes in MRI and MRS signals, which precede clinical signs of disease, could provide insights into the pathogenesis of this disease and may enable early detection of pathology.

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Section: Discussionmentioning

confidence: 99%