Archives Italiennes De Biologie最新文献

During late stages, retinal degenerative disorders affecting photoreceptors progress independently from the specific disease trigger. In fact, a number of detrimental consequences occur downstream of photoreceptors, which are triggered by the loss of photoreceptors themselves. Such downstream anatomical alterations were originally thought to be compensatory events aimed to restore retinal function. At present, these phenomena are deciphered as detrimental effects and the term retinal degeneration is used to indicate the loss of cells and architecture within the inner retina as a consequence of damage to photoreceptors. In the process of testing a photoreceptor-dependent downstream spreading of neurodegeneration we applied a neurotoxin mimicking Parkinson's disease (PD), 1-methyl, 4-phenyl, 1,2,3,6-tetrahydropyridine (MPTP). Chronic MPTP administration produces degeneration within the mouse retina. This is evident by apoptosis quite circumscribed to photoreceptors, which is reminiscent of most phenotypes of retinal degeneration. Retinal pathology following plain HE histochemistry is more widespread with delamination and loss of neuronal packaging in the inner retina. The retinal damage is characterized by a marked synucleinopathy mostly within retinal ganglion cells. In contrast, dopamine-containing structures are intact while norepinephrine is significantly reduced. Despite the involvement of the retina in PD is documented, no study so far analyzed the onset of a synucleinopathy and a degenerative process mimicking what is now recognized in typical retinal degeneration. The present data provide a novel vista on the reciprocal role of the retina in neurodegenerative disorders.

Background: Previous studies have suggested that item memory is processed based on both familiarity and recollection, and evidence can be found from behavioral as well as event-related potential (ERP) patterns. Recently, great consideration has been given to how the memory of items generated from internal and external sources differ from each other. To date, the modulation of fluency, perceptual fluency in particular, on item memory has been rarely explored from both behavioral and neural perspectives. To address these issues, an ERP experiment was conducted.

Methods: Stimuli were encoded in the status of perceived vs. imagined, of either high or low frequency, manipulated by times of exposure (once or twice). Subsequent memory for the items was tested, during which ERP signals were recorded.

Results and conclusion: The findings of the old/new effects reveal the distinctiveness between perceived and imagined items, and demonstrate an influence of fluency, with higher accuracy for items of high fluency than those low fluent ones. The sensitivity of item memory to fluency was discussed in terms of the dual-process model, together with other possible accounts.

In the course of age-related macular degeneration (AMD) as well as in multiple retinal disorders protein aggregates are described at various levels in the retina. In AMD this fills the space between retinal pigment epithelium (RPE) in the form of drusen, which contains amyloid and other protein aggregates along with lipids. Nonetheless, in very advanced stages of AMD, as well as in other retinal pathologies and early on in retinitis pigmentosa, a number of neuronal inclusions, which stain for α-synuclein spreads all over the retinal layers. Thus, an early or later defect in the clearance of α-synuclein may represent a final common pathway to these phenomena. The physiological clearance of α-synuclein is provided by the autophagy machinery starting at the level of the RPE and occurring throughout the retina. Such a process is also involved in the clearance of melanin-dependent toxic metabolites under the effects of different wavelengths and the stimulatory activity of the sympathetic nervous system. In search for the occurrence of these culprits, here we report the presence of α-synuclein in the retina combined with exosomal detection to document the presence of a α-synuclein spreading apparatus. This was correlated with the occurrence of autophagy markers throughout retinal layers, along with sympathetic innervation, which in turn was related to melanin content.

Objective: This preliminary study aims at investigating the neural correlates of the stress response, intended as an emotional and cognitive response, through the description of the activation of the autonomic nervous system in a problem-solving task and central functional data; in particular, we recorded skin conductance level (SCL) and response (SCR) and observed the correlation with fMRI data.

Materials and methods: The results obtained from 6 healthy subjects, 3 males and 3 females, aged between 18 and 45 (average = 27, SD = 7.08) who voluntarily offered to participate in the study were examined. They were previously subjected to a brief clinical psychological assessment (MMPI-2) and then to a psychophysiological evaluation. The real experiment consisted in subjecting the participants to an adapted version of the Raven's Coloured Progressive Matrices 47 (CPM 47) test to evaluate some consequences on brain activity of attention, orientation, reflex and response to stress during fMRI data acquisition and SCL-SCR recording.

Results: SCR changes were found to be related to the activity of different brain regions such as bilateral precentral gyrus, right inferior frontal gyrus, right medial frontal gyrus, bilateral superior frontal gyri and left anterior cingulate suggesting a specific relationship between attentive processing and autonomic arousal.

Conclusion: The association of SC measurement with neuroimaging allows to highlight the interaction between emotional and cognitive processes: although preliminary, these results partially confirm what previously found in literature on the neural correlates of psychological stress and underline the interaction between cognitive function and autonomic arousal system during a stressful problem-solving task.

Age-related macular degeneration (AMD) is a common retinal disorder, which became more and more prevalent in the last decades. AMD is now the most prevalent cause of blindness in the western world. The disorder is classified into two phenotypes named dry and wet AMD. This is based on the recruitment of novel blood vessels and inflammatory exudates in wet AMD. In both phenotypes, the pathological hallmark is the presence of proteinaceous aggregates called drusen, which mostly accumulate between the choroid and the retinal pigment. Drusen in dry AMD represent the evident pathological finding although they are present, though less defined, in wet AMD. In AMD drusen are supposed to be a pathogenic trigger of the disorder. In fact, drusen may mechanically alter retinal function. A novel hypothesis exists, suggesting that a metabolic defect (systemic or focal within the retinal pigment epithelium) may be the real determinant of visual impairment, while causing the concomitant accumulation of proteinaceous debris and lipids forming the drusen. Here we face such an issue by analyzing the retinal anatomy to correlate visual impairment with the occurrence of drusen number, size and the extent of a drusenoid area in the foveal region. A comparison is made with wet AMD where new vessels and retinal exudates prevail. The study is carried out in 120 patients affected by dry or wet AMD and 21 patients where paradoxical findings are described. The main question consists in inferring whether the occurrence of visual impairment is due, in fact, to a drusen-dependent mechanical damage or drusen just occurs as an independent consequence of an upstream metabolic alteration, which concomitantly impairs the visual process. The present data indicate that, despite a significant difference in visual function between mild and severe AMD patients in the amount of drusen exists, a strong correlation between drusen and visual impairment does not occur. This suggests that drusen and visual deterioration develop as a consequence of similar upstream biochemical alterations but it is likely that drusen do not produce visual deterioration. This is strengthened here by extreme clinical conditions, where visual impairment is severe with a slight alteration in the planar pattern of the retina or, vice versa an extended drusenoid area occurs concomitantly with fair visual acuity, contrast sensitivity and lack of metamorphopsia. A biochemical analysis of key areas in the function of specific domains in the pigment epithelium as described in the accompanying manuscript should help to better disclose the real morpho-functional deficit, which takes place in AMD.

In the present study we performed a transcriptional analysis in order to evaluate changes in gene expression induced by exploration in prolonged times. The analysis was carried out 3, 10 and 20 days after exploration. We analyzed the modulation of the expression levels of Pfn2, Casp3, Pdrg1, Pea15, Ywhaz genes which previously were found not modulated 2 days after exploration. Our data show that the expression of Pfn2, Casp3, Pdrg1, Pea15, Ywhaz genes was modulated at 10 or 20 days. The transcript, whose expression had been evaluated with the qRT-PCR, code for proteins which belong to the following functional categories: synaptic modulation, apoptosis, signal transduction. It is interesting to note that the modulation of the expression of these genes was evident some days after environmental exploration, and not previously at 2 days after conditioning as occurred after contextual fear conditioning (CFC). Hence it is possible to hypothesize that the spatial memory processes require a longer period of elaboration than the emotional ones, fundamental for the survival of the species.

Posterior fossa tumors (PFTs) include medulloblastomas, atypical teratoid/rhabdoid tumors, pilocytic astrocytomas, ependymomas, and brainstem gliomas. We evaluated patients with surgery at our clinic, comparing epidemiological, clinical, radiological, and pathological characteristics of medulloblastoma and ependymoma to identify factors that might assist preoperative diagnosis, help to develop treatment algorithms, and have prognostic value after surgery. Pediatric patients from 0 to 16 and young adults from 16 to 29 years of age with surgery for pathologically confirmed ependymomas or medulloblastomas between January 2014 and January 2020 were eligible. The study included 19 patients, seven with ependymoma (37%) and 12 with medulloblastoma (63.2%). The ependymoma patients were 5.29 ± 5.85 years of age, the medulloblastoma patients were 11.58 ± 8.17 years of age, and 16 patients (84%) were children.Fifteen patients (79%) presented with signs of increased intracranial pressure and four (21%) presented with cerebellar findings. MRI found that 74% (14) of the PSTs were located in the midline, including six of the seven ependymomas (86%) and eight of the 12 medulloblastomas (67%). Enhancement was significantly greater in medulloblastomas compared with ependymomas (p = 0.022). In according to pathology results; synaptophysin, NSE, chromogranin and 50% GFAP positivity were observed in medulloblastoma. Ependymomas were S100 (43%) and vimentin (29%) positive. Ependymoma patients were younger than medulloblastoma patients and more were female. There were no significant differences in the clinical findings, but ependymomas were larger and had greater rates of enhancement and spinal metastasis compared with medulloblastomas.

Hyperostosis frontalis interna (HFI) represents an abnormality of the frontal cranial bone that is characterized by bilateral, nodular thickening of its inner lamina and may sometimes be associated with neuropsychiatric symptoms such as headaches and depression. The aim was to assess prevalence, sex and age differences of HFI and frontal bone thickness by means of MRI. This retrospective study included 908 subjects who were divided into male and female groups and further subdivided into three groups, youngest (≤45 years), middle-aged (46- 65 years) and the oldest group (65 years). The thickness of the frontal bone was measured on the T2-weighted axial images at the top level of the lateral ventricles as a mean from both sides. We considered 10mm or thicker frontal bone as HFI. The total prevalence of HFI was 8.1%, with a more frequent occurrence in women (p0.05). In males, there was no difference in the frontal bone thickness between different age groups (p0.05), while in females we found differences between the youngest and the oldest group, and also between the middle-aged and the oldest group (p0.05). The female respondents had a thicker frontal bone, which was statistically significant only in the oldest group (p0.001). Frontal bone thickness was age-dependent only in women (Spearman's Rho 0.11; p≤0.01). In women, unlike in men, there is an age-related progression of HFI with increasing prevalence, with 16.4% occurrence in the oldest group.

This study was aimed to examine the effects of caffeic acid phenethyl ester (CAPE) on endothelial dysfunction in rats with exercise-induced oxidative stress. Tests were performed on male (n=32) young adult Sprague-Dawley rats (12 weeks of age). The experimental animals were divided into four groups in equal numbers. Group 1: General control group; Group 2: Swimming control group. Group 3: CAPE supplemented general control group. Group 4: CAPE supplemented swimming group. Furthermore, animals used in the experiment were made to do exhaustion practice toward the end of the examination. Plasma and liver tissue asymmetric dimethylarginine (ADMA) concentrations were not significantly (p0.05) increased in rats with acute swimming exercise compared to controls. Blood and liver cytokines levels were expanded in comparison to control group and CAPE groups (p0.05). Total antioxidant status (TAS) levels in acute swimming exercise groups reduced compared to the control group. Besides, total oxidant status (TOS) levels were considerably elevated compared to the control and CAPE groups. In this study, acute swimming exercise induced that oxidative stress could cause early onset of endothelial damage. Besides, CAPE can demonstrate protective effects on endothelial damage, inflammation and oxidative stress axis.