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1.
A population of tyrosine hydroxylase (TH)-containing neurons that is up-regulated after lesion of the nigrostriatal dopaminergic pathway has been described in the primate striatum. The goal of this study was to examine the morphology, synaptology, and chemical phenotype of these neurons and TH-immunoreactive (-ir) terminals in the striatum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated rhesus monkeys. TH-ir perikarya were small (10-12 microm), displayed nuclear invaginations, and received very few synaptic inputs. On the other hand, TH-containing dendrites were typically large in diameter (>1.0 microm) and received scarce synaptic innervation from putative excitatory and inhibitory terminals forming asymmetric and symmetric synapses, respectively. More than 70% of TH-positive intrastriatal cell bodies were found in the caudate nucleus and the precommissural putamen, considered as the associative functional territories of the primate striatum. Under 10% of these cells displayed calretinin immunoreactivity. TH-ir terminals rarely formed clear synaptic contacts, except for a few that established asymmetric axodendritic synapses. Almost two-thirds of TH-containing boutons displayed gamma-aminobutyric acid (GABA) immunoreactivity in the striatum of parkinsonian monkeys, whereas under 5% did so in the normal striatum. These findings provide strong support for the existence of a population of putative catecholaminergic interneurons in the associative territory of the striatum in parkinsonian monkeys. Their sparse synaptic innervation raises interesting issues regarding synaptic and nonsynaptic mechanisms involved in the regulation and integration of these neurons in the striatal microcircuitry. Finally, the coexpression of GABA in TH-positive terminals in the striatum of dopamine-depleted monkeys suggests dramatic neurochemical changes in the catecholaminergic modulation of striatal activity in Parkinson's disease. 相似文献
2.
Three experiments are presented in which dopamine (DA) responses from superfused striatal tissue of orchidectomized (ORCH) mice treated or not with testosterone (T) are compared. In experiment 1, potassium-stimulated DA output was significantly greater in ORCH vs. ORCH+T mice. This profile was reversed when reserpine was infused in experiment 2, with DA output being significantly greater in ORCH+T vs. ORCH mice. In experiment 3, the amount of DA recovered following infusion of DA indicated no statistically significant differences in DA recoveries between ORCH and ORCH+T mice as tested in this paradigm. The findings that both potassium- and reserpine-induced DA responses are altered significantly by T suggests that one potential site of T action might involve the storage/uptake of DA within the vesicles of these neurons. Such results have important implications with regard to understanding the sex differences that are present in nigrostriatal dopaminergic function within health and diseased states. 相似文献
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4.
Eilhard Mix Oliver Schmitt Désirée Dräger Reiner Benecke Andreas Wree 《Journal of neuroscience research》2013,91(6):838-847
Botulinum neurotoxin (BoNT) inhibits the release of acetylcholine from presynaptic vesicles through its proteinase activity cleaving the SNARE complex. Parkinson's disease (PD) is associated with locally increased cholinergic activity in the striatum. Therefore, the present study investigates the effect of unilateral intrastriatal BoNT‐A injection in naïve rats on striatal morphology; i.e., the total number of Nissl‐stained neurons and the volume of caudate‐putamen (CPu) were estimated. Furthermore, stainings for markers of gliosis (glial fibrillary acidic protein) and microglia (Iba1) were performed. In addition, the potential beneficial effects of a unilateral intrastriatal injection of BoNT‐A on motor activity in the rat model of hemi‐PD were evaluated. Hemi‐PD was induced by unilateral injection of 6‐hydroxydopamine (6‐OHDA) into the right medial forebrain bundle. Six weeks later, rats received an ipsilateral intrastriatal injection of BoNT‐A. Behaviorally, motor performance was tested. The total number of CPu neurons and the striatal volume were not significantly different between the BoNT‐A‐injected right and the intact left hemispheres of naïve rats. In hemi‐PD rats, intrastriatal BoNT‐A abolished apomorphine‐induced rotations, increased amphetamine‐induced rotations, and tended to improve left forelimb usage. Forced motor function in the accelerod test was not significantly changed by BoNT‐A, and open field activity was also unaltered compared with sham treatment. Thus, intrastriatal BoNT‐A affects spontaneous motor activity of hemi‐PD rats to a minor degree compared with drug‐induced motor function. In the future, tests assessing the cognitive and emotional performance should be performed to ascertain finally the potential therapeutic usefulness of intrastriatal BoNT‐A for PD. © 2013 Wiley Periodicals, Inc. 相似文献
5.
Michelle J Porritt Ann E Kingsbury Andrew J Hughes David W Howells 《Movement disorders》2006,21(12):2208-2211
Increased numbers of dopaminergic neurons are described in the striatum of patients with Parkinson's disease. In postmortem striatal tissue from Parkinson's disease patients with short disease duration (< or =8 years), the number of dopaminergic neurons is approximately four times that in patients with long duration (> or =16 years). The data suggest the possibility that the presence of large numbers of these striatal dopaminergic neurons may be harmful and may accelerate the disease process. Alternatively, these neurons may be lost to the disease process. 相似文献
6.
Bàrbara Segura PhD Hugo César Baggio MD Maria Josep Marti MD PhD Francesc Valldeoriola MD PhD Yaroslau Compta MD PhD Anna Isabel Garcia‐Diaz PhD Pere Vendrell PhD Núria Bargallo MD PhD Eduardo Tolosa MD PhD Carme Junque PhD 《Movement disorders》2014,29(12):1495-1503
The aim of this study was to investigate patterns of cortical atrophy associated with mild cognitive impairment in a large sample of nondemented Parkinson's disease (PD) patients, and its relation with specific neuropsychological deficits. Magnetic resonance imaging (MRI) and neuropsychological assessment were performed in a sample of 90 nondemented PD patients and 32 healthy controls. All underwent a neuropsychological battery including tests that assess different cognitive domains: attention and working memory, executive functions, memory, language, and visuoperceptual‐visuospatial functions. Patients were classified according to their cognitive status as PD patients without mild cognitive impairment (MCI; n = 43) and PD patients with MCI (n = 47). Freesurfer software was used to obtain maps of cortical thickness for group comparisons and correlation with neuropsychological performance. Patients with MCI showed regional cortical thinning in parietotemporal regions, increased global atrophy (global cortical thinning, total gray matter volume reduction, and ventricular enlargement), as well as significant cognitive impairment in memory, executive, and visuospatial and visuoperceptual domains. Correlation analyses showed that all neuropsychological tests were associated with cortical thinning in parietotemporal regions and to a lesser extent in frontal regions. These results provide neuroanatomic support to the concept of MCI classified according to Movement Disorders Society criteria. The posterior pattern of atrophy in temporoparietal regions could be a structural neuroimaging marker of cognitive impairment in nondemented PD patients. All of the neuropsychological tests reflected regional brain atrophy, but no specific patterns were seen corresponding to impairment in distinct cognitive domains. © 2014 International Parkinson and Movement Disorder Society 相似文献
7.
Chromaffin cells grafted to the brain of animals with experimental parkinsonism and patients with Parkinson's disease can restore nigrostriatal functions. Mechanisms underlying these beneficial effects are unknown, but may include growth factors rather than the minute amounts of dopamine (DA) liberated from chromaffin cells. We now report that protein from chromaffin granules, which release their contents by exocytosis, promotes survival and uptake of 3H-DA of mesencephalic DAergic neurons in vitro and protect against N-methylpyridinium ion toxicity. This neurotrophic effect is accompanied by cell proliferation and mediated by astroglial cells induced in these cultures. Inhibition of cell proliferation and concomitant astrogliosis by 5-fluorodeoxyuridine and α-aminoadipic acid abolishes the trophic effect. Two highly specific inhibitors of the epidermal growth factor receptor (EGFR) signal transduction pathway, 4,5-dianilinophthalimide (10 μM) and tyrphostin B56 (10 μM), selectively block the neurotrophic capacity of chromaffin granule protein. As expected, they also block the mitogenic effects of EGF and TGF-α. However, these two mitogens do not mimic the pronounced mitogenic and trophic actions of chromaffin granule protein. Culture medium conditioned by mesencephalic cells pretreated with chromaffin granule protein promotes survival of DAergic neurons without increasing numbers of astroglial cells. The effective molecule is unlikely to be glial cell line-derived neurotrophic factor, whose mRNA is not detectable in cultures treated with chromaffin granule protein. We conclude that chromaffin granules contain a putatively novel growth factor, which signals through the EGFR and may be responsible for the known protective and restorative actions of chromaffin cell grafts to the lesioned nigrostriatal system. J. Neurosci. Res. 48:18–30, 1997. © 1997 Wiley-Liss, Inc. 相似文献
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Dean E Dluzen Linda I Anderson Janet L McDermott Jan Kucera Jon M Walro 《Synapse (New York, N.Y.)》2002,43(2):112-117
We reported previously that mice lacking one brain-derived neurotrophic factor (BDNF) allele demonstrate elevated striatal dopamine (DA) concentrations but impaired behavioral responses involving the nigrostriatal dopaminergic (NSDA) system. To test the hypothesis that these elevated striatal DA concentrations are associated with perturbed NSDA functioning, we compared striatal DA output between heterozygous mutant (+/-) and wild-type littermate control (+/+) BDNF mice under conditions of an intact NSDA system, as well as following methamphetamine (MA)-induced neurotoxicity. Basal DA output from superfused CS tissue fragments did not differ between +/+ and +/- BDNF mice. Potassium (K+) stimulated DA outputs from intact striatal fragments of +/+ mice were significantly greater than that of +/- BDNF mice. Following MA treatment, K+ stimulated DA output of +/+ mice was statistically equivalent to +/- BDNF mice. Striatal DA concentrations of +/- BDNF mice were elevated, albeit not significantly, in both intact and MA-treated mice relative to +/+ mice. Following MA treatment, striatal DA concentrations were significantly decreased for both genotypes; however, the degree of DA depletion was significantly greater in +/+ mice. Analyzed collectively, these data show the differential effects exerted by a BDNF mutation upon striatal DA concentrations and output. Notably, lower striatal DA concentrations of +/+ vs. +/- BDNF mice can be contrasted with the significantly greater K+ stimulated DA output from the former. This difference was abolished following MA treatment. These results suggest that processes involved with the dynamics of DA release within the NSDA system may be compromised in +/- BDNF mutant mice. 相似文献
9.
Barcia C Sánchez Bahillo A Fernández-Villalba E Bautista V Poza Y Poza M Fernández-Barreiro A Hirsch EC Herrero MT 《Glia》2004,46(4):402-409
Inflammatory changes have been found in Parkinson's disease, in humans intoxicated with the parkinsonian toxin MPTP, and in animal models of the disease. However, it is still not known whether inflammatory changes are responsible for active nerve cell death or if they have a protective role against neurodegeneration. In this study, we analyzed the glial reaction in the substantia nigra pars compacta (SNpc) and the striatum of monkeys rendered parkinsosian by chronic MPTP injections. At postmortem examination 1 year after the last MPTP injection, the density of astroglial cells and activated microglial cells in the SNpc, but not in the striatum, of MPTP-intoxicated animals was significantly higher than in the two control animals. These data suggest that neurodegeneration was still active despite the absence of the agent triggering cell death and that the glial reaction is associated with long-term neurodegeneration. 相似文献
10.
Peter T. Bell Moran Gilat Claire O'Callaghan David A. Copland Michael J. Frank Simon J.G. Lewis James M. Shine 《Human brain mapping》2015,36(4):1278-1291
The pathological hallmark of Parkinson's disease is the degeneration of dopaminergic nigrostriatal neurons, leading to depletion of striatal dopamine. Recent neuroanatomical work has identified pathways for communication across striatal subdivisions, suggesting that the striatum provides a platform for integration of information across parallel corticostriatal circuits. The aim of this study was to investigate whether dopaminergic dysfunction in Parkinson's disease was associated with impairments in functional connectivity across striatal subdivisions, which could potentially reflect reduced integration across corticostriatal circuits. Utilizing resting‐state functional magnetic resonance imaging (fMRI), we analyzed functional connectivity in 39 patients with Parkinson's disease, both “on” and “off” their regular dopaminergic medications, along with 40 age‐matched healthy controls. Our results demonstrate widespread impairments in connectivity across subdivisions of the striatum in patients with Parkinson's disease in the “off” state. The administration of dopaminergic medication significantly improved connectivity across striatal subdivisions in Parkinson's disease, implicating dopaminergic deficits in the pathogenesis of impaired striatal interconnectivity. In addition, impaired striatal interconnectivity in the Parkinson's disease “off” state was associated with pathological decoupling of the striatum from the thalamic and sensorimotor (SM) networks. Specifically, we found that although the strength of striatal interconnectivity was positively correlated with both (i) the strength of internal thalamic connectivity, and (ii) the strength of internal SM connectivity, in both healthy controls and the Parkinson's disease “on” state, these relationships were absent in Parkinson's disease when in the “off” state. Taken together our findings emphasize the central role of dopamine in integrated striatal function and the pathological consequences of striatal dopamine denervation in Parkinson's disease. Hum Brain Mapp 36:1278–1291, 2015. © 2014 Wiley Periodicals, Inc . 相似文献
11.
Monoamine-activated alpha-2-macroglobulin (α2M) has been shown to decrease the dopamine concentrations in rat caudate putamen (CP) in vivo as well as inhibit choline acetyltransferase activities in the culture of basal forebrain neurons. In this study, we further investigated the effects of methylamine-activated α2M (MA-α2M) upon striatal rlopaminergic function by determining whether a direct infusion of this glycoprotein will alter dopamine (DA) release in vitro from superfused CP tissue fragments. In experiment 1, an infusion of 2.8 μM MA-α2M produced a statistically significant increase in DA release compared with control superfusions. In experiment 2, varying doses (0, 0.7, 1.4, 2.8, 4.1 μM) of MA-α2M were tested for their capacity to alter DA release. Only the 2.8 μM dose of MA-α2M was effective in producing a significant increase of DA release. In experiment 3, the normal form of α2M (N-α2M) at 2.8 μM was compared with the control superfusions. The infusion of N-α2M produced an increase in DA release which was substantially lower than the DA increase induced by MA-α2M, and not significantly different from that of the control superfusion. These results show that MA-α2M, like some other neurotoxins, can markedly alter CP dapaminergic function as indicated by the acute increase in DA release following infusion of this glycoprotein, and these effects are exerted at a relatively narrow range of doses. Taken together, these data suggest that this glycoprotein, if allowed to accumulate in the central nervous system (CNS), may promote some neurodegenerative changes that can occur in disorders like Parkinson's disease. © 1996 Wiley-Liss, Inc. 相似文献
12.
Naroa Ibarretxe‐Bilbao PhD Carme Junque PhD Barbara Segura PhD Hugo C. Baggio MD Maria J. Marti MD PhD Francesc Valldeoriola MD PhD Nuria Bargallo MD PhD Eduardo Tolosa MD PhD 《Movement disorders》2012,27(14):1746-1753
The aim of this study was to investigate the progression of cortical thinning and gray‐matter (GM) volume loss in early Parkinson's disease (PD). MRI and neuropsychological assessment were obtained at baseline and follow‐up (mean ± standard deviation = 35.50 ± 1.88 months) in a group of 16 early‐PD patients (H & Y stage ≤II and disease duration ≤5 years) and 15 healthy controls matched for age, gender, and years of education. FreeSurfer software was used for the analysis of cortical thickness as well as for cortical and subcortical volumetric analyses. Voxel‐based morphometry analysis was performed using SPM8. Compared to controls, PD patients showed greater regional cortical thinning in bilateral frontotemporal regions as well as greater over‐time total GM loss and amygdalar volume reduction. PD patients and controls presented similar over‐time changes in cognitive functioning. In early‐PD patients, global GM loss, amygdalar atrophy, and cortical thinning in frontotemporal regions are specifically associated with the PD‐degenerative process. © 2012 Movement Disorder Society 相似文献
13.
Chul Hyoung Lyoo MD PhD Young Hoon Ryu MD PhD Myung Sik Lee MD PhD 《Movement disorders》2010,25(4):496-499
The pathology of Parkinson's disease (PD) is not confined to the brainstem regions, but spreads to involve the neocortical areas. Using surface‐based cortical thickness analysis, we studied the topographical distribution of cortical thinning in nondemented patients with mild PD. The high‐resolution magnetic resonance imaging (MRI) studies were performed in 48 patients with PD without dementia and 56 age‐matched healthy controls. Using the Freesurfer software, surface‐based analysis was done to find changes in cerebral cortical thickness in patients with PD. Compared to the controls, patients with PD showed significant cortical thinning in the temporal, inferior parietal, rostral frontal, and orbitofrontal cortical areas. Thinning of the cerebral cortex occurs even in nondemented patients with mild PD, and its topographical distribution was similar to that of the neocortical Lewy bodies. Further studies are needed to find pathological and clinical correlates of thinned cerebral cortex found in nondemented patients with mild PD. © 2010 Movement Disorder Society 相似文献
14.
Muñoz AM Rey P Soto-Otero R Guerra MJ Labandeira-Garcia JL 《Journal of neuroscience research》2004,76(4):551-562
The results of several in vitro studies have shown that cysteine prodrugs, particularly N-acetylcysteine, are effective antioxidants that increase the survival of dopaminergic neurons. N-acetylcysteine can be systemically administered to deliver cysteine to the brain and is of potential use for providing neuroprotection in the treatment of Parkinson's disease. However, it has also been reported that an excess of cysteine may induce neurotoxicity. In the present study, we injected adult rats intrastriatally with 2.5 microl of 6-hydroxydopamine (7.5 microg) and N-acetylcysteine (240 mM) or cysteine (240 mM) or intraventricularly with 6-hydroxydopamine (200 microg) and subcutaneously with N-acetylcysteine (10 and 100 mg/kg). We studied the effects of these compounds on both the nigrostriatal dopaminergic terminals and the surrounding striatal tissue. The tissue was stained with fluoro-jade (a marker of neuronal degeneration) and processed by immunohistochemistry to detect tyrosine hydroxylase, neuronal and glial markers, and the stress protein heme-oxygenase-1. After intrastriatal injection, both cysteine and N-acetylcysteine had clear neuroprotective effects on the striatal dopaminergic terminals, but also led to neuronal degeneration (as revealed by fluoro-jade staining) and astroglial and microglial activation, as well as intense induction of heme-oxygenase-1 in astrocytes and microglial cells. Subcutaneous administration of N-acetylcysteine also induced significant reduction of the dopaminergic lesion (about 30% reduction). However, we did not observe appreciable N-acetylcysteine-induced fluoro-jade labeling in striatal neurons or any of the above-mentioned changes in striatal glial cells. The results suggest that low doses of cysteine prodrugs may be useful neuroprotectors in the treatment of Parkinson's disease. 相似文献
15.
Chao Wang Cheng Zhou Tao Guo Yeerfan Jiaerken Siyu Yang Peiyu Huang Xiaojun Xu Minming Zhang 《CNS Neuroscience & Therapeutics》2023,29(10):2800-2810
Background
Mounting studies have demonstrated that coffee consumption significantly reduces the risk of developing Parkinson's disease (PD). However, there have been few investigations about the role of chronic coffee consumption in nigrostriatal structural neurodegeneration in PD. We aimed to investigate whether chronic coffee consumption is associated with the change in striatal volume in PD.Methods
In this study, 130 de novo patients with PD and 69 healthy controls were enrolled from the Parkinson's Progression Markers Initiative cohort. Patients with PD and healthy controls were, respectively, divided into three subgroups, including current, ever, and never coffee consumers. Then, striatal volume was compared across the three subgroups. Correlation analyses were performed to assess the relationship between cups consumed per day and striatal volume. Furthermore, we included the factors that may have influenced nigrostriatal dopaminergic neurons in multiple linear regression analyses to identify significant contributing factors to striatal volume in each investigated striatal region.Results
Current coffee consumers had decreased striatal volume compared with ever consumers in controls but not patients with PD. Furthermore, the correlation analyses revealed that cups per day were negatively correlated with striatal volume in current consumers of patients with PD and controls. In addition, multiple linear regression analyses showed that current coffee consumption remained as an independent predictor of a decrease in striatal volume in controls.Conclusions
Our study showed that chronic coffee consumption was negatively correlated with striatal volume. In addition, our study showed that chronic coffee consumption was associated with the change in striatal volume in current—rather than ever coffee consumers, which suggests that the chronic effects of caffeine on striatal morphology may fade and even compensate after quitting coffee. Our study provides evidence for the effect of chronic coffee consumption on striatal volume in human brain in vivo. 相似文献16.
Flavio Nobili MD Claudio Campus PhysD Dario Arnaldi MD Fabrizio De Carli PsyD Gaia Cabassi PhysD Andrea Brugnolo PsyD Barbara Dessi PsyD Silvia Morbelli MD Gianmario Sambuceti MD Giovanni Abbruzzese MD Guido Rodriguez MD 《Movement disorders》2010,25(1):35-43
To unveil cognitive‐nigrostriatal correlations in Parkinson's disease (PD), 30 de novo, drug‐naïve PD patients and 15 patients with essential tremor (Controls, CTR) underwent a neuropsychological (NPS) battery and brain SPECT with [I‐123]Ioflupane, as a biomarker of nigrostriatal function. Automatic extraction of uptake at caudate and putamen level was conducted through the BasGan software, also allowing partial volume effect correction. Because of the multicollinearity among neuropsychological tests and among SPECT variables, factor analysis was applied to 16 neuropsychological scores; moreover, the four SPECT variables were merged into a mean SPECT value (mSPECT). Factor analysis identified four NPS factors: a dys‐executive (NPS‐EX), a visuospatial (NPS‐VS), a verbal memory (NPS‐VM), and a “mixed” (NPD‐MIX) factor. In PD group, there were inverse correlations between UPDRS‐III score and both NPS‐VS (P < 0.01) and mSPECT (P < 0.05), and a direct correlation between mSPECT and NPS‐EX (P < 0.05). Post hoc analysis showed a direct correlation between NPS‐EX and caudate uptake in both hemispheres (P < 0.05). Moreover, inverse correlations were found between UPDRS‐III and, respectively, putamen uptake in the less affected hemisphere (P < 0.01), and putamen and caudate uptake in the more affected hemisphere (P < 0.05). In CTR, no correlation was found between mSPECT and either NPS or GDS values. Nigro‐caudate function affects executive capabilities in PD but not in CTR, which appears to be unrelated to the disease motor severity at its onset. Instead, PD motor severity is related to nigro‐putaminal impairment and visuospatial dysfunction. The role of these data as predictive features of cognitive decline and eventually dementia remains to be established in longitudinal studies. © 2010 Movement Disorder Society 相似文献
17.
To determine whether the adenosine A2A receptor might play a role in L-DOPA-induced dyskinesia in Parkinson's disease, we analyzed changes in the expression of A2A receptor mRNA in response to intermittent treatment with L-DOPA in rats with dopaminergic denervation by 6-hydroxydopamine (OHDA) infusion into the medial forebrain bundle. Intermittent treatment with L-DOPA increased A2A receptor mRNA levels in the dopamine-depleted striatum of 6-OHDA-lesioned rats exhibiting behavioral sensitization to L-DOPA. These results suggest that A2A receptor activation is associated with the development of motor complications induced by L-DOPA treatment. 相似文献
18.
Michelle Porritt Davor Stanic David Finkelstein Peter Batchelor Sharon Lockhart Andrew Hughes Renate Kalnins David Howells 《Movement disorders》2005,20(7):810-818
In Parkinson's disease (PD), dopaminergic input to the caudate nucleus and a band of putaminal tissue abutting the external globus pallidus seems well preserved on immunohistochemical staining for the dopamine transporter. Counting of dopaminergic terminals showed that terminal density in these regions in PD was the same as that in controls, which indicates that input is truly preserved and not a consequence of a compensatory upregulation of metabolism in a reduced pool of surviving terminals. When the branching pattern of dopaminergic axons coursing through the globus pallidus was examined, we found no evidence for increased axonal sprouting in PD that might have contributed to preservation of dopaminergic input to the putamen or caudate nucleus. Although terminal counting indicated that anatomic input was preserved to parts of the striatum, dopamine uptake site density in these regions was reduced significantly. This suggests that the impact of disease in these areas is more profound than was thought previously. 相似文献
19.
Background : Functional connectivity is abnormal in PD and in early Alzheimer's disease. Objectives : The objective of this study was to evaluate resting‐state striato‐cortical connectivity in PD and Alzheimer's disease and assess their relation to cognitive outcomes. Groups with mild cognitive impairment as a result of different pathologies (PD vs. Alzheimer's disease) were also compared. Methods : Seed‐based connectivity of the dorsal, middle, and ventral striatum was analyzed in 111 patients using functional MRI. The correlation between connectivity at regions of between‐group differences and clinical outcomes was assessed. Results : Patients showed lower striatal connectivity than controls. Connectivity between the middle (associative) striatum and precuneus negatively correlated with executive functions in PD and with memory performance in Alzheimer's disease. PD with cognitive impairment showed decreased connectivity of the dorsal (motor) striatum when compared with early Alzheimer's disease. Conclusions : Striatal connectivity was reduced in patients when compared with controls. Similar compensatory mechanisms were employed to overcome various cognitive deficits in PD and Alzheimer's disease. © 2017 International Parkinson and Movement Disorder Society 相似文献
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