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Environmental exposure to metallic neurotoxicants is a matter of growing concern since it may have very significant consequences for human health, from impairing neurodevelopment in children to the neurodegeneration processes involved in aging. The scientific community will face many challenges in identifying and preventing the adverse effects of environmental metal exposure on brain health. This collection of articles provides an overview of current work in the field of neurotoxicology of metal contaminants, from the identification of emerging toxic compounds, to the assessment of environmental exposures and associated risks, through the description of the molecular mechanisms involved in neurotoxicity.

Medicine --- Medical toxicology --- Alzheimer’s disease --- copper --- soil and water pollution --- heavy metals --- morels --- grasspea --- cassava --- neurodegeneration --- mitochondrial dysfunction --- neurological disorders --- metals --- neurotoxicity --- arsenic --- Alzheimer’s disease (AD) --- environmental risk factor --- proteostasis --- apoptosis --- phytochemicals --- grip strength --- neuromotor system --- NHANES --- synapse --- metal --- cadmium --- lead --- manganese --- mercury --- methylmercury --- diet --- cholesterol --- high fat --- low fat --- manganese speciation --- SH-SY5Y --- protein metabolism --- metal-on-metal (MoM) hip implants --- cobalt --- systemic cobaltism --- RNA-Seq --- RT-qPCR --- environmental exposure --- cognitive function --- race --- ethnicity --- CERAD --- animal fluency --- DSST --- n/a --- Alzheimer's disease --- Alzheimer's disease (AD)

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Environmental exposure to metallic neurotoxicants is a matter of growing concern since it may have very significant consequences for human health, from impairing neurodevelopment in children to the neurodegeneration processes involved in aging. The scientific community will face many challenges in identifying and preventing the adverse effects of environmental metal exposure on brain health. This collection of articles provides an overview of current work in the field of neurotoxicology of metal contaminants, from the identification of emerging toxic compounds, to the assessment of environmental exposures and associated risks, through the description of the molecular mechanisms involved in neurotoxicity.

Medicine --- Medical toxicology --- Alzheimer's disease --- copper --- soil and water pollution --- heavy metals --- morels --- grasspea --- cassava --- neurodegeneration --- mitochondrial dysfunction --- neurological disorders --- metals --- neurotoxicity --- arsenic --- Alzheimer's disease (AD) --- environmental risk factor --- proteostasis --- apoptosis --- phytochemicals --- grip strength --- neuromotor system --- NHANES --- synapse --- metal --- cadmium --- lead --- manganese --- mercury --- methylmercury --- diet --- cholesterol --- high fat --- low fat --- manganese speciation --- SH-SY5Y --- protein metabolism --- metal-on-metal (MoM) hip implants --- cobalt --- systemic cobaltism --- RNA-Seq --- RT-qPCR --- environmental exposure --- cognitive function --- race --- ethnicity --- CERAD --- animal fluency --- DSST --- Alzheimer's disease --- copper --- soil and water pollution --- heavy metals --- morels --- grasspea --- cassava --- neurodegeneration --- mitochondrial dysfunction --- neurological disorders --- metals --- neurotoxicity --- arsenic --- Alzheimer's disease (AD) --- environmental risk factor --- proteostasis --- apoptosis --- phytochemicals --- grip strength --- neuromotor system --- NHANES --- synapse --- metal --- cadmium --- lead --- manganese --- mercury --- methylmercury --- diet --- cholesterol --- high fat --- low fat --- manganese speciation --- SH-SY5Y --- protein metabolism --- metal-on-metal (MoM) hip implants --- cobalt --- systemic cobaltism --- RNA-Seq --- RT-qPCR --- environmental exposure --- cognitive function --- race --- ethnicity --- CERAD --- animal fluency --- DSST

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Positron emission tomography (PET) and single-photon emission computed tomography (SPECT) are in vivo molecular imaging methods which are widely used in nuclear medicine for diagnosis and treatment follow-up of many major diseases. These methods use target-specific molecules as probes, which are labeled with radionuclides of short half-lives that are synthesized prior to the imaging studies. These probes are called radiopharmaceuticals. The use of PET and SPECT for brain imaging is of special significance since the brain controls all the body’s functions by processing information from the whole body and the outside world. It is the source of thoughts, intelligence, memory, speech, creativity, emotion, sensory functions, motion control, and other important body functions. Protected by the skull and the blood–brain barrier, the brain is somehow a privileged organ with regard to nutrient supply, immune response, and accessibility for diagnostic and therapeutic measures. Invasive procedures are rather limited for the latter purposes. Therefore, noninvasive imaging with PET and SPECT has gained high importance for a great variety of brain diseases, including neurodegenerative diseases, motor dysfunctions, stroke, epilepsy, psychiatric diseases, and brain tumors. This Special Issue focuses on radiolabeled molecules that are used for these purposes, with special emphasis on neurodegenerative diseases and brain tumors.

Research & information: general --- Biology, life sciences --- SV2A --- SV2B --- SV2C --- microPET --- [18F]UCB-H --- epilepsy --- PBIF --- distribution volume --- blocking assay --- preclinical imaging --- Alzheimer’s disease (AD) --- network measure --- graph theory --- brain network --- positron emission tomography (PET) --- persistent homology --- Phosphodiesterase 2A (PDE2A) --- Positron Emission Tomography (PET) --- Benzoimidazotriazine (BIT) --- fluorinated --- Mouse Liver Microsomes (MLM) --- cyclic nucleotide phosphodiesterase --- PDE2A radioligand --- nitro-precursor --- fluorine-18 --- in vitro autoradiography --- PET imaging --- opioid receptors --- positron emission tomography --- radiotracers --- μOR-, δOR-, κOR- and ORL1-ligands --- movement disorders --- pain --- drug dependence --- GBM --- biomarkers --- Sigma 1 --- Sigma 2 --- PD-L1 --- PARP --- IDH --- Alzheimer’s disease --- Parkinson’s disease --- β-amyloid plaques --- neurofibrillary tangles --- α-synucleinopathy --- diagnostic imaging probes --- orexin receptors --- PET --- radiotracer --- imaging --- alpha 7 --- nicotinic acetylcholine receptors --- nAChR --- autoradiography --- amino acid --- FET --- FACBC --- FDOPA --- immunoPET --- molecular imaging --- glioma --- brain metastases --- adenosine A2A receptor --- rotenone-based mouse model --- [18F]FESCH --- two-step one-pot radiosynthesis

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This reprint combines recent original manuscripts and reviews covering the multiple functions of peroxisome proliferator-activated receptors in physiology and pathophysiology. Potential applications and limitations of PPAR agonists and antagonists are discussed. All original contributions were published in Cells.

peroxisome-proliferator activated receptors --- tumor angiogenesis --- tumor progression --- metastasis formation --- endothelial cells --- RNA sequencing --- PPARs --- toxicology --- pharmacology --- ligand --- vascular --- coronary artery --- lipidomics --- eicosanoids --- inflammation --- CYP450 --- peroxisome proliferator-activated receptor --- angiogenesis --- proliferation --- metastasis --- immortality --- resistance to cell death --- growth suppressors --- immune system --- cellular metabolism --- PPAR --- nuclear receptors --- addiction --- alcohol --- nicotine --- opioids --- psychostimulants --- animal models --- human studies --- Alzheimer’s --- risk factors --- PPARα --- lipids --- fatty acids --- modulators --- cognition --- sex --- therapy --- hypertrophic adipocytes --- PPARG isoforms --- PPARG splicing --- dominant-negative isoform --- in vitro adipocytes --- adipogenesis --- hypertrophic obesity --- insulin-resistance --- peroxisome proliferator-activated receptors (PPARs) --- synthetic agonists --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- fibrosis --- Sirtuin1 --- peroxisome proliferator-activated receptor-γ coactivator-1α --- peroxisome proliferator activated receptors --- obesity --- metabolic syndrome --- vitamin B12 --- folate --- fetal programming --- inherited metabolic disorders --- PGC-1α, disease --- kidney --- cancer --- AKI --- CKD --- nephron --- PKD --- cilia --- cystogenesis --- ligands --- Alzheimer’s disease (AD)

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This reprint combines recent original manuscripts and reviews covering the multiple functions of peroxisome proliferator-activated receptors in physiology and pathophysiology. Potential applications and limitations of PPAR agonists and antagonists are discussed. All original contributions were published in Cells.

Medicine --- Physiology --- peroxisome-proliferator activated receptors --- tumor angiogenesis --- tumor progression --- metastasis formation --- endothelial cells --- RNA sequencing --- PPARs --- toxicology --- pharmacology --- ligand --- vascular --- coronary artery --- lipidomics --- eicosanoids --- inflammation --- CYP450 --- peroxisome proliferator-activated receptor --- angiogenesis --- proliferation --- metastasis --- immortality --- resistance to cell death --- growth suppressors --- immune system --- cellular metabolism --- PPAR --- nuclear receptors --- addiction --- alcohol --- nicotine --- opioids --- psychostimulants --- animal models --- human studies --- Alzheimer’s --- risk factors --- PPARα --- lipids --- fatty acids --- modulators --- cognition --- sex --- therapy --- hypertrophic adipocytes --- PPARG isoforms --- PPARG splicing --- dominant-negative isoform --- in vitro adipocytes --- adipogenesis --- hypertrophic obesity --- insulin-resistance --- peroxisome proliferator-activated receptors (PPARs) --- synthetic agonists --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- fibrosis --- Sirtuin1 --- peroxisome proliferator-activated receptor-γ coactivator-1α --- peroxisome proliferator activated receptors --- obesity --- metabolic syndrome --- vitamin B12 --- folate --- fetal programming --- inherited metabolic disorders --- PGC-1α, disease --- kidney --- cancer --- AKI --- CKD --- nephron --- PKD --- cilia --- cystogenesis --- ligands --- Alzheimer’s disease (AD) --- peroxisome-proliferator activated receptors --- tumor angiogenesis --- tumor progression --- metastasis formation --- endothelial cells --- RNA sequencing --- PPARs --- toxicology --- pharmacology --- ligand --- vascular --- coronary artery --- lipidomics --- eicosanoids --- inflammation --- CYP450 --- peroxisome proliferator-activated receptor --- angiogenesis --- proliferation --- metastasis --- immortality --- resistance to cell death --- growth suppressors --- immune system --- cellular metabolism --- PPAR --- nuclear receptors --- addiction --- alcohol --- nicotine --- opioids --- psychostimulants --- animal models --- human studies --- Alzheimer’s --- risk factors --- PPARα --- lipids --- fatty acids --- modulators --- cognition --- sex --- therapy --- hypertrophic adipocytes --- PPARG isoforms --- PPARG splicing --- dominant-negative isoform --- in vitro adipocytes --- adipogenesis --- hypertrophic obesity --- insulin-resistance --- peroxisome proliferator-activated receptors (PPARs) --- synthetic agonists --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- fibrosis --- Sirtuin1 --- peroxisome proliferator-activated receptor-γ coactivator-1α --- peroxisome proliferator activated receptors --- obesity --- metabolic syndrome --- vitamin B12 --- folate --- fetal programming --- inherited metabolic disorders --- PGC-1α, disease --- kidney --- cancer --- AKI --- CKD --- nephron --- PKD --- cilia --- cystogenesis --- ligands --- Alzheimer’s disease (AD)