Manoj Kumar Jaiswal, Ph.D

Affiliations: 
2009-2010 Brain and Cognitive Sciences Massachusetts Institute of Technology, Cambridge, MA, United States 
 2015-2017 Molecular Imaging and Neuropathology Columbia / New York State Psychiatric Institute 
 2017- Psychiatry Icahn School of Medicine at Mount Sinai, New York, NY, United States 
Area:
Cellular Neuroscience, Calcium Imaging, Motoneuron disease, ALS, Synaptic trnasmission
Website:
http://www.mountsinai.org/profiles/manoj-k-jaiswal
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"Manoj Jaiswal"
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Publications

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Jaiswal MK. (2020) Therapeutic opportunities and challenges of induced pluripotent stem cells-derived motor neurons for treatment of amyotrophic lateral sclerosis and motor neuron disease. Neural Regeneration Research. 12: 723-736
Jaiswal MK. (2017) Riluzole But Not Melatonin Ameliorates Acute Motor Neuron Degeneration and Moderately Inhibits SOD1-Mediated Excitotoxicity Induced Disrupted Mitochondrial Ca2+ Signaling in Amyotrophic Lateral Sclerosis Frontiers in Cellular Neuroscience. 10: 295
Aizenstein HJ, Baskys A, Boldrini M, et al. (2016) Vascular depression consensus report - a critical update. Bmc Medicine. 14: 161
Paine A, Jaiswal MK. (2016) Promise and Pitfalls of Mitochondrial Replacement for Prevention and Cure of Heritable Neurodegenerative Diseases Caused by Deleterious Mutations in Mitochondrial DNA. Frontiers in Cellular Neuroscience. 10: 219
Jaiswal MK. (2014) Motoneuron specific calcium dysregulation and perturbed cellular calcium homestasis in amyotrophic lateral sclerosis: Recent advances gained from genetically modified animals and cell culture models Motor Neuron Diseases: Causes, Classification and Treatments. 75-102
Jaiswal MK. (2013) Calcium, mitochondria, and the pathogenesis of ALS: the good, the bad, and the ugly. Frontiers in Cellular Neuroscience. 7: 199
Jaiswal MK, Zech WD, Goos M, et al. (2009) Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron disease. Bmc Neuroscience. 10: 64
Jaiswal MK, Keller BU. (2009) Cu/Zn superoxide dismutase typical for familial amyotrophic lateral sclerosis increases the vulnerability of mitochondria and perturbs Ca2+ homeostasis in SOD1G93A mice. Molecular Pharmacology. 75: 478-89
Goos M, Zech WD, Jaiswal MK, et al. (2007) Expression of a Cu,Zn superoxide dismutase typical for familial amyotrophic lateral sclerosis increases the vulnerability of neuroblastoma cells to infectious injury. Bmc Infectious Diseases. 7: 131
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