Is neurodegenerative disease a long-latency response to early-life genotoxin exposure? - Test2 - elhamkhani - TriplyDB

Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

http://www.wikidata.org/entity/Q26824755

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A global perspective on the influence of environmental exposures on the nervous system Unraveling 50-Year-Old Clues Linking Neurodegeneration and Cancer to Cycad Toxins: Are microRNAs Common Mediators?Animal models of brain maldevelopment induced by cycad plant genotoxins Health-based cyanotoxin guideline values allow for cyanotoxin-based monitoring and efficient public health response to cyanobacterial blooms.Hippocampal developmental vulnerability to methylmercury extends into prepubescence.Comorbidities in Neurology: Is adenosine the common link?Interrelationships of undernutrition and neurotoxicity: food for thought and research attention.Cassava food toxins, konzo disease, and neurodegeneration in sub-Sahara Africans Presence of the neurotoxin BMAA in aquatic ecosystems: what do we really know?Estrogen receptor β and Liver X receptor β: biology and therapeutic potential in CNS diseases.A critical review of the postulated role of the non-essential amino acid, β-N-methylamino-L-alanine, in neurodegenerative disease in humans.L-BMAA induced ER stress and enhanced caspase 12 cleavage in human neuroblastoma SH-SY5Y cells at low nonexcitotoxic concentrations.Tobacco Smoke Exposure Impairs Brain Insulin/IGF Signaling: Potential Co-Factor Role in Neurodegeneration.Accrued somatic mutations (nucleic acid changes) trigger ALS: 2005-2015 update.Longitudinal Study-Based Dementia Prediction for Public Health.β-N-Methylamino-L-alanine (BMAA) perturbs alanine, aspartate and glutamate metabolism pathways in human neuroblastoma cells as determined by metabolic profiling.Western Pacific ALS-PDC: a prototypical neurodegenerative disorder linked to DNA damage and aberrant proteogenesis?Investigating β-N-Methylamino-l-alanine Misincorporation in Human Cell Cultures: A Comparative Study with Known Amino Acid Analogues.ALSUntangled 38: L-serine

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P2860

Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

http://www.wikidata.org/entity/Q26824755

description

2011 nî lūn-bûn

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2011 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2011 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

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Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

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Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

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Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

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Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

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Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

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Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

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Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

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Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

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International Journal of Environmental Research and Public Health

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Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?

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Glen E. Kisby

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Peter S. Spencer

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Creative Commons Attribution 3.0 Unported

P2860

Neuroinflammation – An Early Event in Both the History and Pathogenesis of Alzheimer’s Disease

Early environmental origins of neurodegenerative disease in later life.

The cycad genotoxin MAM modulates brain cellular pathways involved in neurodegenerative disease and cancer in a DNA damage-linked manner

Biomagnification of cycad neurotoxins in flying foxes: implications for ALS-PDC in Guam

Clinical features and changing patterns of neurodegenerative disorders on Guam, 1997-2000

Genotoxicity of streptozotocin

Neurotoxicity of beta-N-methylamino-L-alanine (BMAA) and beta-N-oxalylamino-L-alanine (BOAA) on cultured cortical neurons

A mechanism for slow release of biomagnified cyanobacterial neurotoxins and neurodegenerative disease in Guam

Odor identification deficit of the parkinsonism-dementia complex of Guam: equivalence to that of Alzheimer's and idiopathic Parkinson's disease

Occurrence of beta-methylamino-l-alanine (BMAA) in ALS/PDC patients from Guam

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3889-921

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scholarly article

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10.3390/IJERPH8103889

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2011-10-01T00:00:00Z

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22073019

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neurodegeneration

Chin-hu̍t seng-bu̍t

amyotrophic lateral sclerosis

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3210588

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