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Parvathi Menon

Researcher at University of Sydney

Publications -  76
Citations -  2522

Parvathi Menon is an academic researcher from University of Sydney. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Transcranial magnetic stimulation. The author has an hindex of 26, co-authored 70 publications receiving 1849 citations. Previous affiliations of Parvathi Menon include Royal Brisbane and Women's Hospital & Westmead Hospital.

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Pathophysiological and diagnostic implications of cortical dysfunction in ALS

TL;DR: Changes in cortical function that develop in ALS could prove useful as diagnostic biomarkers, potentially enhancing the diagnosis of ALS at an early stage of the disease process and providing potential for more-effective management of patients with ALS.
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Sensitivity and specificity of threshold tracking transcranial magnetic stimulation for diagnosis of amyotrophic lateral sclerosis: a prospective study

TL;DR: The threshold tracking TMS technique reliably distinguishes ALS from non-ALS disorders and, if these findings are replicated in larger studies, could represent a useful diagnostic investigation when combined with the Awaji criteria to prove upper motor neuron dysfunction at early stages of ALS.
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TDP-43 proteinopathies: a new wave of neurodegenerative diseases.

TL;DR: This review highlights the key physiological functions of the TDP-43 protein, while considering an expanding spectrum of neurodegenerative diseases associated with pathogenic T DP-43 deposition, and dissecting key molecular pathways through which TD-43 may mediate neurodegenersation.
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Rate of disease progression: a prognostic biomarker in ALS

TL;DR: Rate of disease progression appears to be a simple and sensitive clinical prognostic biomarker in ALS that could be potentially utilised in clinical practice and future therapeutic trials.
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Cortical hyperexcitability precedes lower motor neuron dysfunction in ALS.

TL;DR: The findings in the present study suggest that cortical hyperexcitability occurs upstream to a seemingly intact lower motor neuronal system in sporadic amyotrophic lateral sclerosis, suggesting a cortical origin of the disease.