4,344 research outputs found
Frontal executive function, apathy and behaviour in parkinson's disease
No full textThe pattern of cognitive deficits in Parkinson's disease is variable, but often includes executive impairment similar to that seen in patients with frontal lesions, as well as episodic memory impairment, visuospatial dysfunction and impaired verbal fluency. That could derive from the not irrelevant "new" role of the basal ganglia in determining cognitive process refinement. We discuss a huge number of pathological observations, starting from neuro-anatomical and biochemical networks, from basal ganglia to thalamus and cortical cortex
Non-motor aspects of parkinson's disease
No full textFor many decades, PD was regarded as a unique entity, namely a sporadic neurodegenerative disease with its main lesion in the substantia nigra. The actual pathology was described as pathognomonic Lewy bodies in nigral dopaminergic cells, and the clinical abnormalities were thought to be due to insufficient dopamine release from nigrostriatal terminals, primarily in the putamen. It is now realized that the classical stereotypic description of PD starting with tremor or hypokinesia/rigidity and progressing to postural instability and eventually to cognitive decline is not the only scenario (although it may be the more common one). This latter observation led to a definition of the "Lewy body dementia" concept where motor symptoms may be minimal initially. In many patients, the disease starts with autonomic (particularly gastro-intestinal) or sensory (i.e., olfactory) manifestations. The identification of a-synuclein as a key constituent of Lewy bodies allowed the demonstration of specific changes in other areas such as the olfactory bulb and particularly the brain stem. Changes in the raphe nucleus and the locus coeruleus which antedate the substantia nigra lesions could explain some mental manifestations, particularly the depression which has been described prior to the first motor manifestations. Several behavioral disorders may be observed in people with PD. Hypodopaminergic states linked to the disease itself or associated with low levodopa levels may frequently contribute to symptoms such as anxiety, apathy, fatigue, sleep disruption. About twothirds of PD patients with fluctuations reported significant "on-off" mood swings. The excessive use of dopaminergic treatment may eventually lead to a pervasive behavioral syndrome termed homeostatic hedonistic dysregulation (HHD). We discuss these aspects with a particular interest in clinical practice
Freezing in-on and parkinson's disease: Cognition and behavior
No full textFreezing of gait (FOG) refers to transient episodes, usually lasting seconds, in which a patient is unable to initiate or continue locomotion, occurring on a background of relatively good ability to move and is best described by patients as "feet get glued to the ground." Freezing of gait is common in Parkinson's disease, with increasing prevalence as the disease progresses, but it has been commonly reported in pathologically proven progressive supranuclear palsy and vascular parkinsonism. Two types of freezing of gait have been recognized in patients affected by Parkinson's Disease, taking L-Dopa. The most common is an "off" -freezing of gait, which can be improved with L-Dopa or dopaminergic treatment, such as apomorphine. "Off" -freezing appears during an "off" state, when the patient is generally bradykinetic and rigid. In contrast, "on" -freezing is characterized by a worsening of symptoms as the dose of L-Dopa is increased, and by a general improvement, as the dose is decreased or, better said, modulated. The onfreezing of gait is related to abnormal execution of complex motor tasks such as repetitive, simultaneous, or sequential motor acts. Different Authors suggested that the primary underlying abnormality might be related to the inability to deliver, or hold a pre-programmed, continuous, and complex motor act, in response to an established and correct internal plan of action. Therefore, we hypothesized that PD- on freezing patients might be clinically well differentiated from the other clinical subtypes of PD and might present a specific cognitive impairment, different from that presented by PD patients, without on-FOG. We discuss these hypothesis, based on clinical studies and follow-up
Parkinson's disease as a model of basal ganglia disruption
No full textThe assumption that the PD neurodegenerative process begins in the dopaminergic substantia nigra has been seriously challenged by recent publications. New different studies have provided evidence in support of a lower brainstem origin, predating involvement of the nigra. In addition to the prominent loss of nigro-striatal dopamine neurons, there is also degeneration of nor-epinephrine neurons in the locus coeruleus, cholinergic neurons in the nucleus basalis of Meynert, the dorsal motor nucleus of the vagus, and involvement of the spinal cord and peripheral autonomic system. There is dysfunction of multiple neurotransmitter systems and research is underway to determine if therapeutic restoration of these transmitters can provide benefit in PD. We discuss these biochemical and pathological aspects inside the most classic clinical assumption of PD as a dopaminergic depletion-induced diseas
Apathy and parkinson's disease
No full textApathy is a pathology of voluntary action or goal-directed behavior (GDB) and the underlying mechanism(s) responsible for apathy may be seen as dysfunctions occurring at the level of elaboration, execution and control of GDB. Apathy is often present after direct lesions of the prefrontal cortex (PFC), but it is also a common clinical feature of basal ganglia diseases. It can be observed in neurodegenerative diseases such as Parkinson's disease or as progressive supranuclear palsy and Huntington's disease. Apathy is also frequently encountered after focal lesions of specific structures of the basal ganglia such as the caudate nuclei, the internal pallidum and the medial-dorsal thalamic nuclei. Apathy is therefore one of the clinical consequences of the disruption of the PFC-basal ganglia axis, one of the functional systems involved in the generation and control of self-generated purposeful behaviour. From this perspective, a prefrontal-like syndrome (including apathy as one of its clinical manifestations) can be encountered following diseases that mainly involve the basal ganglia. This suggests that apathy can also be the consequence of a 'prefrontal-like' syndrome due to lesions mostly affecting the basal ganglia. Therefore, we try to define the apathy importance in PD, and even in different clinical phenotype profiles of PD
La Collezione Vicino Orientale del Museo Barracco di Roma nei cataloghi d’asta dell’Hôtel Drouot
No full textThis article focuses on the historical framework of the Italian and French collectors, with special regard to the collection at the Barracco Museum.
This is specifically analyzed with reference to its relation with the near-eastern regions and its role in the Parisian art market. The
research conducted in auction catalogs of the Hôtel Drouot has allowed us to gather new information on the collection. Thus, starting with verified reports and records taken from the collection, it was possible to identify new data regarding G. Barracco’s acquaintances and his purchases, which were probably conducted through intermediaries.
In particular, a special relevance is attached to an Assyrian relief whose origin was previously unknown in scholarly literature and that the author identifies as a part of the Barracco collection thanks to a mention in one of the Drouot catalogs
Filologia editoriale, Roberto Calasso in dialogo con Paola Italia e Francisco Rico
No full textPaola Italia e Francisco Rico intervengono sul libro di Roberto Calasso, presidente e fondatore di Adelphi Edizioni, L'impronta dell'editore, e discutono di problemi di filologia delle forme editoriali, dal punto di vista dell'autore, del lettore e dell'editore.Paola Italia and Francisco Ricos interview Roberto Calasso, Publisher, Writer, and Founder of Adelphi Edizioni, about his book: L'impronta dell'editore, talking about philology, publishing and editing, from the author, the reader and the publisher's point of view
Paola Gianturco: Women Who Light the Dark
No full textPaola Gianturco is a photographer, author, and advocate for women\u27s rights world-wide. For the past thirteen years, she has worked as a photojournalist, documenting women’s lives in forty countries. She has published four acclaimed photo books which bring together inspiring stories with gorgeous photographs to motivate her readers to engage with, learn from and support women around the world. All of Gianturco’s books are philanthropic projects, for which she donates her royalties to carefully selected nonprofit organizations that relate to each book\u27s content. Paola\u27s most recent book, Women Who Light the Dark, tells the story of local women around the world who are helping one another tackle the problems that darken their lives—including violence, poverty, illiteracy and disease. Gianturco is giving 100% of her author royalties for this book to The Global Fund for Women.https://thekeep.eiu.edu/humanitiescenter_meaningfulwork1011/1002/thumbnail.jp
Participación del lóbulo temporal en la consolidación y reconsolidación de la extinción del condicionamiento de aversión al sabor /
No full text\ua0tesis que para obtener el grado de Doctor en Ciencias Biomédicas, presenta Paola García de la Torre ; asesor Federico Bermúdez Rattoni, Alicia Elizabeth Hernández Echeagaray, Oscar Prospéro García. 62 páginas :\ua0diagramas. Doctorado en Ciencias Biomédicas\ua0UNAM, Instituto de Fisiología Celular,\ua0201
NETosis in pathologies: a preliminary study for NETs detection in vitro
No full textBackground: Neutrophils are the major participants in NETosis, a novel kind of regulated cell death (RCD) that has recently emerged. As a result, neutrophils not only serve as the initial line of defense for the host, but they also help to mediate the new RCD by releasing neutrophil extracellular traps (NETs).1 NETosis is characterized by sequence of events: intracellular membranes disintegrate and proteases from granules enter the nucleus, followed by hypercitrullination of histones, chromatin decondensation and extrusion of nuclear material from the cell. Then, NETs decorated by decondensed chromatin, modified histones and granular enzymes are released from cells. 2
Physiologically, NETs entrap bacteria and provide a natural defence against inflammation but an exacerbated release of NETs markers can exert pro-thrombotic and pro-inflammatory effects and are resulted implicated in many diseases such as hyperglycaemia, diabetes and its complications. 3
Aim: The project has the purpose to to study in depth NETosis pathway and its implications in pathogenesis. Specifically, will be characterize the epi-modulation of NETs formation in samples derived from cancer and diabetic patients.
Materials and methods: differentiation of HL60 FOR 5 days with Dimethyl sulfoxide or All-trans retinoic acid. May Grunwald Giemsa staining. Immunofluorescence staining Anti-MPO and H3cit. Flow based assay to detect NETs. ROS assay.
Result: several methods have been developed o investigate NETosis. NETs formation has been identified after epi drugs induction.
The methods we are using to detect NETs and to evaluate NETosis markers are efficient to study NETosis in blood samples from patients.
Conclusions: NETosis is a recent discovered RCD that resulted de-regulated in many pathologies. The characterization of NETosis mechanism and complete understanding of NETosis role in pathogenesis could provide new prognostic markers and novels therapeutic targets
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