مرحله بندی پاتولوژی مغز مربوط به بیماری پارکینسون پراکنده
|کد مقاله||سال انتشار||تعداد صفحات مقاله انگلیسی||ترجمه فارسی|
|31049||2003||15 صفحه PDF||سفارش دهید|
نسخه انگلیسی مقاله همین الان قابل دانلود است.
هزینه ترجمه مقاله بر اساس تعداد کلمات مقاله انگلیسی محاسبه می شود.
این مقاله تقریباً شامل 10203 کلمه می باشد.
هزینه ترجمه مقاله توسط مترجمان با تجربه، طبق جدول زیر محاسبه می شود:
- تولید محتوا با مقالات ISI برای سایت یا وبلاگ شما
- تولید محتوا با مقالات ISI برای کتاب شما
- تولید محتوا با مقالات ISI برای نشریه یا رسانه شما
پیشنهاد می کنیم کیفیت محتوای سایت خود را با استفاده از منابع علمی، افزایش دهید.
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Neurobiology of Aging, Volume 24, Issue 2, March–April 2003, Pages 197–211
Sporadic Parkinson’s disease involves multiple neuronal systems and results from changes developing in a few susceptible types of nerve cells. Essential for neuropathological diagnosis are α-synuclein-immunopositive Lewy neurites and Lewy bodies. The pathological process targets specific induction sites: lesions initially occur in the dorsal motor nucleus of the glossopharyngeal and vagal nerves and anterior olfactory nucleus. Thereafter, less vulnerable nuclear grays and cortical areas gradually become affected. The disease process in the brain stem pursues an ascending course with little interindividual variation. The pathology in the anterior olfactory nucleus makes fewer incursions into related areas than that developing in the brain stem. Cortical involvement ensues, beginning with the anteromedial temporal mesocortex. From there, the neocortex succumbs, commencing with high order sensory association and prefrontal areas. First order sensory association/premotor areas and primary sensory/motor fields then follow suit. This study traces the course of the pathology in incidental and symptomatic Parkinson cases proposing a staging procedure based upon the readily recognizable topographical extent of the lesions.
Sporadic Parkinson’s disease (PD) is a progressive degenerative illness of the human nervous system that manifests itself clinically after the pathology already has reached an advanced stage ,  and . A prerequisite for the post-mortem diagnosis of both the presymptomatic and symptomatic phases of the pathological process underlying PD is evidence of specific inclusion bodies, which develop as spindle- or thread-like Lewy neurites (LNs) in cellular processes, and in the form of globular Lewy bodies (LBs) in neuronal perikarya , ,  and . In sporadic PD, only a few specific types of nerve cells are prone to develop the lesions. A major component of LNs and LBs is an aggregated form of the normally presynaptic protein α-synuclein. It is still unknown why this hydrophilic protein leaves its binding sites within synaptic boutons and, together with other components such as phosphorylated neurofilaments and ubiquitin, a heat shock protein required for the non-lysosomal ATP-dependent breakdown of abnormal proteins, gradually transforms into virtually insoluble LNs or LBs , , , , , , ,  and . Damage to specific subnuclei of the substantia nigra, pars compacta, with severe obliteration of their neuromelanin-laden projection neurons, frequently is considered to be the most important hallmark of PD , , ,  and . The nigral damage, however, always is accompanied by extensive extranigral pathology, including that in the dorsal motor nucleus of the glossopharyngeal and vagal nerves (i.e. dorsal IX/X motor nucleus) and adjoining intermediate reticular zone, in some subnuclei of the reticular formation and the raphe system, the coeruleus–subcoeruleus complex, the magnocellular nuclei of the basal forebrain, and many subnuclei of the thalamus and amygdala. Cases with severe damage usually show lesions reaching the neocortex , , , , ,  and . The question arises as to whether the pathology evolves simultaneously at all of these nigral and extranigral induction sites or whether the various sites differ in their susceptibilities to develop the disease-related alterations and, accordingly, follow a coherent sequence. The present study, therefore, intentionally includes a spectrum of cases exhibiting LNs and LBs in a specific subset of neuronal types and predilection sites, which are known to be involved in clinical PD cases. In doing so, we assume it to be correct that nonsymptomatic and symptomatic cases can be ordered in such a manner that cases exhibiting the mildest pathology represent the starting point and those most heavily involved the terminus of a disease spectrum, with a tendency toward increasing severity on the part of the overall pathology (Table 2). According to this assumption, the neuronal damage does not develop randomly but, rather, follows a predetermined sequence marked by characteristic changes in topographical extent. The present study is aimed at working out a neuropathological staging procedure based upon the topography of these changes. It is not our intent here to correlate the proposed neuropathological stages with clinical symptoms. Furthermore, we would like to emphasize that the study sample does not include cases clinically diagnosed as diffuse LB disease. Likewise, we did not detail study cases which were neuropathologically classified as fully-developed Alzheimer’s disease (AD) with co-occurring LBs and LNs in prosencephalic areas. It remains to be seen whether deviations from the proposed staging scheme exist in cases of advanced AD with LBs or in cases of clinically assessed diffuse LB disease.