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Matthew Gregory Lewis (Londra, 9 luglio – Oceano Atlantico, 14 maggio ) è stato un romanziere e drammaturgo britannico, famoso per il suo romanzo gotico Il monaco. . Crea un libro · Scarica come PDF · Versione stampabile. the monk by matthew gregory lewis. Mon, 25 Mar GMT the monk by matthew gregory pdf - The. Monk: A Romance is gotico Il monaco. Tue, The Monk: A Romance is a Gothic novel by Matthew Gregory Lewis, published in romanziere e drammaturgo britannico, famoso per il suo romanzo gotico Il monaco. Free sheet music CELLO - VIOLONCELLO - Download PDF, MP3.
PD with dementia PDD strikingly reduces the quality of life of PD patients, enormously enhances financial burdens for their families and greatly causes life stresses for their caregivers.
However, roles of above pathological proteins on PD-CI are not fully understood yet. Neuroinflammation characterized by microglial activation serves as an engine driving PD progression.
Recently, the significance of neuroinflammation in PD pathology extends beyond substantia nigra and neuroinflammation impairs regions relevant to non-motor symptoms [ 6 ]. However, there are few investigations on the role of neuroinflammation in the development and progression of PD with cognitive impairment PD-CI and the relationship between the pathological proteins and neuroinflammation in PD-CI is unclear yet.
Oxidative stress featured by the robust productions of highly toxic free radicals plays a pivotal role on cognitive decline in human with neurodegenerative diseases and PD animal model. An animal experiment shows positive correlations of spatial memory deficits with indicators of oxidative stress in rat PD model treated with lipopolysaccharide alone or plus 6-hydroxydopamine [ 7 ].
Lycopene protects against cognitive decline through inhibition of oxidative stress in rotenone-induced PD model [ 8 ]. These data indicate a critical role of oxidative stress on cognitive impairment in neurodegenerative diseases.
However, there is no investigation on the relationships between PD-CI and free radicals in patients. We hypothesize that the deposition of above pathological proteins in cognition-associated regions may, on one hand, activate microglia and produce neuroinflammatory factors, and on the other hand, cause oxidative stress and generate free radicals, leading to neuronal damage and cognitive impairment.
To test this hypothesis, in this study, we assessed cognitive function for PD patients, detected the levels of pathological proteins, neuroinflammatory factors and free radicals in cerebrospinal fluid CSF from PD patients, and analyzed the relationships between cognitive impairment and above factors with aim to figure out the potential mechanisms and biomarkers associated with the development and severity of cognitive impairment in PD patients.
Patients with other primary explanations for cognitive impairment e. We recruited 31 normal controls consecutively based on the following criteria: The average age of control group was matched with that of PD group. Written informed consents were obtained from participants or their guardians if they had dementia. Continuous variables, if they were not normally distributed, were presented as median quartile and compared by nonparametric test. Discrete variables were compared by Chi square test.
In the total 62 PD patients, 36 Control group vs. PD-CI group, P 3: PD-NCI group vs.
PD-CI group. No significant correlations are found between the levels of neuroinflammatory factors or free radicals and the levels of pathological proteins in CSF from PD patients.
In this study, It has high test-retest and inter-rater reliability and is notably correlated with a neuropsychological battery. Based on the scoring rate of all cognitive domains in MoCA from low to high level, dysfunction of vocabulary memory ranks the top in PD-CI patients, which is reported to be associated with hippocampus atrophy [ 13 ].
Abstraction is the second domain impaired significantly, followed by visuospatial and executive function. Disturbances of abstraction and executive function are associated with the impairment of frontal-striatal dopaminergic pathway [ 14 ]. Relationship between executive dysfunction and visuospatial deficit in PD patient is complicated [ 15 ]. Investigators have found that statistically controlling deficits in executive skills through analysis of covariance eliminates visuospatial impairment, implying that executive dysfunction may account for visuospatial impairment in PD subjects, however, statistically controlling visuospatial deficits fails to alter abnormal executive function, indicating that visuospatial dysfunction is independent of executive dysfunction in PD [ 16 ].
Additionally, posterior brain regions are found to be dominant for visuospatial ability [ 17 ]. Evidence shows that a short time to cognitive impairment is associated with old age [ 18 ], which is confirmed by our study. However, we find that educational level in PD-NCI group is higher than that in PD-CI group, which suggests that higher educational has a protective effect against cognitive impairment [ 19 ].
One prospective study fails to find an association between T-tau level in CSF and cognitive decline in PD patients [ 20 ]. Neuroinflammation featured by microglial activation contributes to the cascade events leading to neuronal degeneration in PD [ 23 ].
Neuroinflammatory factors exert toxic effects directly by binding to related receptors and activating second messenger pathways, or indirectly by inducing the expression of cyclooxygenase 2, a PGE 2- generating enzyme [ 23 ], promoting degeneration and death of dopaminergic neurons and subsequent occurrence of motor symptoms.
However, role of neuroinflammation in the occurrence and development of PD-CI is rarely conducted. Aging is a risk factor for both PD and cognitive decline. Neuroinflammation becomes severer with age [ 27 ] and may underlie the cognitive disabilities in PD patients. Chronic inflammatory disease exerts detrimental effects on cognitive function for persons with chronic periodontal inflammation [ 29 ].
High IL-1 level in hippocampus impairs learning ability [ 30 ]. Blocking IL-1 with receptor antagonist or knocking out IL-1 in mice [ 31 ] attenuates cognitive dysfunction. These data imply a potential correlation between neuroinflammation and cognitive impairment. However, role of neuroinflammation on PD-CI are rarely conducted. A PET scan with PK, a ligand of peripheral binding site of benzodiazepine indicative of microglial activation, reveals neuroinflammation in PD patients [ 32 ].
Cognitive disorders-related cortical regions, including frontal and temporal lobes, have increased binding of PK Another study shows that PDD patients have significantly higher level of C-reactive protein in CSF than non-demented PD patients after controlling for age, gender and somatic illness [ 33 ].
Considering the influence of age on the levels of neuroinflammatory factors in CSF, we made further analyses between IL-6 level in CSF and age in both PD group and PD-CI group, and find no significant correlation, which suggest that the elevated levels of neuroinflammatory factors are not resulted from aging, and are closely associated with PD-CI. Oxidative stress characterized by robust generations of free radicals plays a crucial role on neuronal damage in PD. Upon a variety of stimuli, activation of microglial nicotinamide adenine dinucleotide phosphate oxidase 2, a superoxide-generating enzyme, produces a large amount of superoxide very quickly.
Microglial expression of inducible nitric oxide synthase leads to excessive NO generation [ 23 ]. Previous studies indicate an important role of oxidative stress on cognitive impairment in neurodegenerative diseases [ 7 , 8 , 34 ]; however, less attention is paid to the role of free radicals on PD-CI.
Correlations of the levels of neuroinflammatory factors and free radicals with pathological proteins in CSF in PD patients are not observed in this study. A variety of stimuli can induce neuroinflammation and oxidative stress in brain.
Thus, pathological protein alone may not be sufficient to elicit robust productions of neuroinflammatory factors and free radicals in CSF. We will enhance the sample size of PDD patients and investigate the clinical feature and potential mechanism of dementia in PD patients in the very near future.
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