3篇
您的检索式：作者名="Nady Braidy"
|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Kynurenine pathway metabolism and neuroinflammatory disease显示文摘Immune-mediated activation of tryptophan(TRYP) catabolism via the kynurenine pathway(KP) is a consistent finding in all inflammatory disorders.Several studies by our group and others have examined the neurotoxic potential of neuroreactive TRYP metabolites,including quinolinic acid(QUIN) in neuroinflammatory neurological disorders,including Alzheimer's disease(AD),multiple sclerosis,amylotropic lateral sclerosis(ALS),and AIDS related dementia complex(ADC).Our current work aims to determine whether there is any benefit to the affected individuals in enhancing the catabolism of TRYP via the KP during an immune response.Under physiological conditions,QUIN is metabolized to the essential pyridine nucleotide,nicotinamide adenine dinucleotide(NAD+),which represents an important metabolic cofactor and electron transporter.NAD+ also serves as a substrate for the DNA ‘nick sensor' and putative nuclear repair enzyme,poly(ADP-ribose) polymerase(PARP).Free radical initiated DNA damage,PARP activation and NAD+ depletion may contribute to brain dysfunction and cell death in neuroinflammatory disease. | Nady Braidy Ross Grant | 2017 | Neural Regeneration Research2017，12，1： | 6 |
| 2 | Uptake and mitochondrial dysfunction of alpha-synuclein in human astrocytes, cortical neurons and fibroblasts显示文摘The accumulation and aggregation of alpha-synuclein(α-syn)in several tissue including the brain is a major pathological hallmark in Parkinson’s disease(PD).In this study,we show that α-syn can be taken up by primary human cortical neurons,astrocytes and skin-derived fibroblasts in vitro.Our findings that brain and peripheral cells exposed to α-syn can lead to impaired mitochondrial function,leading to cellular degeneration and cell death,provides additional evidence for the involvement of mitochondrial dysfunction as a mechanism of toxicity of α-syn in human cells. | Nady Braidy Wei-Ping Gai Ying Hua Xu Perminder Sachdev Gilles J Guillemin Xing-Mai Jiang J William O Ballard Martin P Horan Zhi Ming Fang Beng H Chong Daniel Kam Yin Chan | 2013 | Translational Neurodegeneration2013，2，1： | 4 |
| 3 | Mini-review on initiatives to interfere with the propagation and clearance of alphasynuclein in Parkinson’s disease显示文摘In this mini-review,we summarize recent findings relating to the prion-like propagation ofα-synuclein(α-syn)and the development of novel therapeutic strategies to target synucleinopathy in Parkinson’s disease(PD).We link the Braak’s staging hypothesis of PD with the recent evidence from in-vivo and in-vitro studies for the prion-like cell-to-cell propagation ofα-syn(via exocytosis and endocytosis).The classical accumulation of aggregatedα-syn in PD may result from an increased production or a failure in the mechanisms of clearance ofα-syn.We discuss novel agents,currently in clinical trial for PD including the ones that impact the aggregation ofα-syn and others that interfere withα-syn endocytosis as a means to target the progression of the disease. | Daniel Kam Yin Chan Ying Hua Xu Luke Kar Man Chan Nady Braidy George D.Mellick | 2017 | Translational Neurodegeneration2017，6，1： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员