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Cited by 123 publications
(87 citation statements)
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“…In clinical cases of PD, several abnormalities have been detected in areas virtually depleted of Lewy inclusions (FC and CB), including mitochondrial dysfunction, oxidative stress and synaptic pathology. 16,[53][54][55][56][57][58] This suggests that svtRNA2-1a upregulation may be linked to complex molecular pathology rather than to the distribution of Lewy inclusions. Furthermore, our observations indicate that svtRNA2-1a upregulation occurs at early (pre-motor) stages of the disease, thus suggesting a possible role in the initial pathogenic events in PD.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…In clinical cases of PD, several abnormalities have been detected in areas virtually depleted of Lewy inclusions (FC and CB), including mitochondrial dysfunction, oxidative stress and synaptic pathology. 16,[53][54][55][56][57][58] This suggests that svtRNA2-1a upregulation may be linked to complex molecular pathology rather than to the distribution of Lewy inclusions. Furthermore, our observations indicate that svtRNA2-1a upregulation occurs at early (pre-motor) stages of the disease, thus suggesting a possible role in the initial pathogenic events in PD.…”
Section: Discussionmentioning
confidence: 99%
“…Gene expression profiling studies in different brain areas from sporadic PD patients have widely shown transcriptome deregulation affecting these pathways. [9][10][11][12][13][14][15][16] MicroRNAs (miRNAs) and other small non-coding RNAs (sncRNAs) are post-transcriptional gene expression regulators, playing key roles in neuronal development, plasticity and disease. A strong body of evidence suggests that miRNA dysregulation confirmed a significant upregulation of svtRNA2-1a of approximately 1.5-fold in AM from PD compared with control AM (Fig.…”
Section: Intracerebral Formation Of Lbs and Lns Hasmentioning
confidence: 99%
“…Complex I impairment seems to be important for the pathogenesis of PD since exposure to inhibitors of this complex, such as MPP + or rotenone, reproduces the clinical symptoms of PD observed in human subjects [105,106].Complex I is the largest of the electron transport chain (ETC) complexes, consisting of 46 subunits, 7 of which are encoded by mitochondrial DNA (mtDNA) [107]and the major site of superoxide production in the ETC [108]. Complex I activity and expression are decreased in the SN[109Ͳ112] and cortex [113] of PD patients to a greater extent than would be expected from normal aging [107]. Oxidized, functionally impaired and misassembled complex I subunits, have been reported in PD [114].Moreover, complex I dysfunction was reported in skeletal muscle and platelets of PD patients [112].…”
Section: Sources Of Oxidative Damage In Pdmentioning
confidence: 99%
“…Therefore, factors other than the accumulation of abnormal α-synuclein in the form of LB and LN are causative of the abnormal cortical function (17). Molecular neuropathology has elucidated a series of modifications that may result in impaired function of selected metabolic pathways, these including altered mitochondrial function, glycolysis and protein degradation pathways in the frontal cortex in PD and iPD (17,18). There is some agreement that molecular damage in PD is due to oxidative stress, which enhances oxidative DNA damage and increases the expression levels of lipoxidation, nitration and glycoxidation markers and lipid peroxides and increases the expression of RAGE (advanced glycation end products receptor) in the frontal cortex of PD and iPD (19)(20)(21).…”
Section: Introductionmentioning
confidence: 99%