Putaminal petechial haemorrhage as the cause of chorea: a neuroimaging study

Abstract Background Perturbed functional coupling between the metabotropic glutamate receptor-5 (mGluR5) and N-methyl-d-aspartate (NMDA) receptor-mediated excitatory glutamatergic neurotransmission may contribute to the pathophysiology of psychiatric disorders such as schizophrenia. We aimed to establish the functional interaction between mGluR5 and NMDA receptors in brain of mice with genetic ablation of the mGluR5. Methods We first measured the brain glutamate levels with magnetic resonance spectroscopy (MRS) in mGluR5 knockout (KO) and wild-type (WT) mice. Then, we assessed brain glucose metabolism with [18F]fluorodeoxyglucose ([18F]FDG) positron emission tomography before and after the acute administration of an NMDA antagonist, MK-801 (0.5 mg/kg), in the same mGluR5 KO and WT mice. Results Between-group comparisons showed no significant differences in [18F]FDG standardized uptake values (SUVs) in brain of mGluR5 KO and WT mice at baseline, but widespread reductions in mGluR5 KO mice compared to WT mice after MK-801 administration (p < 0.05). The baseline glutamate levels did not differ significantly between the two groups. However, there were significant negative correlations between baseline prefrontal glutamate levels and regional [18F]FDG SUVs in mGluR5 KO mice (p < 0.05), but no such correlations in WT mice. Fisher’s Z-transformation analysis revealed significant between-group differences in these correlations (p < 0.05). Conclusions This is the first multimodal neuroimaging study in mGluR5 KO mice and the first report on the association between cerebral glucose metabolism and glutamate levels in living rodents. The results indicate that mGluR5 KO mice respond to NMDA antagonism with reduced cerebral glucose metabolism, suggesting that mGluR5 transmission normally moderates the net effects of NMDA receptor antagonism on neuronal activity. The negative correlation between glutamate levels and glucose metabolism in mGluR5 KO mice at baseline may suggest an unmasking of an inhibitory component of the glutamatergic regulation of neuronal energy metabolism.

Download Full-text

Relating Reading, Visualization, and Coding for New Programmers: A Neuroimaging Study

2021 IEEE/ACM 43rd International Conference on Software Engineering (ICSE) ◽

10.1109/icse43902.2021.00062 ◽

2021 ◽

Author(s):

Madeline Endres ◽

Zachary Karas ◽

Xiaosu Hu ◽

Ioulia Kovelman ◽

Westley Weimer

Keyword(s):

Neuroimaging Study

Download Full-text

A 4-year Longitudinal Neuroimaging Study of Cognitive Control using Latent Growth Modeling: Developmental Changes and Brain-Behavior Associations

NeuroImage ◽

10.1016/j.neuroimage.2021.118134 ◽

2021 ◽

pp. 118134

Author(s):

Jungmeen Kim-Spoon ◽

Toria Herd ◽

Alexis Brieant ◽

Jacob Elder ◽

Jacob Lee ◽

...

Keyword(s):

Cognitive Control ◽

Growth Modeling ◽

Latent Growth Modeling ◽

Developmental Changes ◽

Latent Growth ◽

Neuroimaging Study ◽

Brain Behavior

Download Full-text

A molecular pathology, neurobiology, biochemical, genetic and neuroimaging study of progressive apraxia of speech

Nature Communications ◽

10.1038/s41467-021-23687-8 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Keith A. Josephs ◽

Joseph R. Duffy ◽

Heather M. Clark ◽

Rene L. Utianski ◽

Edythe A. Strand ◽

...

Keyword(s):

Progressive Supranuclear Palsy ◽

Molecular Pathology ◽

Age At Onset ◽

Haplotype Frequency ◽

Corticobasal Degeneration ◽

Apraxia Of Speech ◽

Speech Characteristics ◽

Biochemical Genetic ◽

Neuroimaging Study ◽

Longitudinal Imaging

AbstractProgressive apraxia of speech is a neurodegenerative syndrome affecting spoken communication. Molecular pathology, biochemistry, genetics, and longitudinal imaging were investigated in 32 autopsy-confirmed patients with progressive apraxia of speech who were followed over 10 years. Corticobasal degeneration and progressive supranuclear palsy (4R-tauopathies) were the most common underlying pathologies. Perceptually distinct speech characteristics, combined with age-at-onset, predicted specific 4R-tauopathy; phonetic subtype and younger age predicted corticobasal degeneration, and prosodic subtype and older age predicted progressive supranuclear palsy. Phonetic and prosodic subtypes showed differing relationships within the cortico-striato-pallido-nigro-luysial network. Biochemical analysis revealed no distinct differences in aggregated 4R-tau while tau H1 haplotype frequency (69%) was lower compared to 1000+ autopsy-confirmed 4R-tauopathies. Corticobasal degeneration patients had faster rates of decline, greater cortical degeneration, and shorter illness duration than progressive supranuclear palsy. These findings help define the pathobiology of progressive apraxia of speech and may have consequences for development of 4R-tau targeting treatment.

Download Full-text