共查询到20条相似文献,搜索用时 31 毫秒
1.
Eiki Takahashi Kimie Niimi Chitoshi Itakura 《Journal of molecular neuroscience : MN》2010,41(2):223-229
It has been reported earlier that interactions between Cav2.1α1 and calcium/calmodulin-dependent protein kinase II (CaMKII) in the presynaptic fraction and between the NMDA receptor subunit
NR2B and CaMKII in the postsynaptic density (PSD) fraction are important for neuronal function. Cav2.1α1, CaMKII, and NR2B are predominantly expressed in the hippocampus. To examine the above interactions and CaMKII activity in
the hippocampal presynapse and PSD of Rolling Nagoya mice carrying a mutation in Cav2.1α1 subunit, we performed immunoprecipitation and Western blot analyses. In the presynapse, the interaction between Cav2.1α1 and CaMKII and the phosphorylation of CaMKII (at Thr286) and its substrate Synapsin I (at Ser603) were decreased in mutant
mice compared to wild-type mice. In the PSD, a similar pattern was observed for the interaction between NR2B and CaMKII and
the phosphorylation of CaMKII (at Thr286) and its substrate AMPA receptor subunit glutamate receptor 1 (at Ser831) between
mutant and wild-type mice. Our data indicate that disruption of the interaction between Cav2.1α1 and CaMKII may down-regulate presynaptic CaMKII activity and that Rolling Nagoya mice would be a useful model for examining presynaptic function. 相似文献
2.
Franco R Lluis C Canela EI Mallol J Agnati L Casadó V Ciruela F Ferré S Fuxe K 《Journal of neural transmission (Vienna, Austria : 1996)》2007,114(1):93-104
Summary. The molecular basis for the known intramembrane receptor–receptor interactions among heptahelical receptors (G protein coupled
receptors, GPCR) was postulated to be heteromerization based on receptor subtype specific interactions between different types
of homomers of GPCR. Adenosine and dopamine receptors in the basal ganglia have been fundamental to demonstrate the existence
of receptor heteromers and the functional consequences of such molecular interactions. The heterodimer is only one type of
heteromeric complex and the evidence is equally compatible with the existence of higher order heteromeric complexes, where
also adapter proteins such as homer proteins and scaffolding proteins can exist, assisting in the process of linking the GPCR
and ion channel receptors together in a receptor mosaic that may have special integrative value and may constitute the molecular
basis for learning and memory. Heteromerization of D2 dopamine and A2A adenosine receptors is reviewed by Fuxe in another article in this special issue. Here, heteromerization between D1 dopamine and A1 adenosine receptors is reviewed. Heteromers formed by dopamine D1 and D2 receptors and by adenosine A1 and A2A receptors also occur in striatal cells and open new perspectives to understand why two receptors with apparently opposite
effects are expressed in the same neuron and in the nerve terminals. The role of accessory proteins also capable of interacting
with receptor–receptor heteromers in regulating the traffic and the molecular physiology of these receptors is also discussed.
Overall, the knowledge of the reason why such complex networks of receptor–receptor and receptor–protein interactions occur
in striatal cells is crucial to develop new strategies to combat neurological and neuropsychiatric diseases. 相似文献
3.
Arturo Reyes-Vaca Lizbeth de la Cruz Julieta Garduño Isabel Arenas David E. Garcia 《Journal of molecular neuroscience : MN》2017,63(3-4):377-384
Voltage-dependent regulation of CaV2.2 channels by G-proteins is performed by the β (Gβ) subunit. Most studies of regulation by G-proteins have focused on channel activation; however, little is known regarding channel inactivation. This study investigated inactivation of CaV2.2 channels in superior cervical ganglion neurons that overexpressed Gβ subunits. CaV2.2 currents were recorded by whole-cell patch clamping configuration. We found that the Gβ1 subunit reduced inactivation, while Gβ5 subunit did not alter at all inactivation kinetics compared to control recordings. CaV2.2 current decay in control neurons consisted of both fast and slow inactivation; however, Gβ1-overexpressing neurons displayed only the slow inactivation. Fast inactivation was restored by a strong depolarization of Gβ1-overexpressing neurons, therefore, through a voltage-dependent mechanism. The Gβ1 subunit shifted the voltage dependence of inactivation to more positive voltages and reduced the fraction of CaV2.2 channels resting in the inactivated state. These results support that the Gβ1 subunit inhibits the fast inactivation of CaV2.2 channels in SCG neurons. They explain the long-observed sustained Ca2+ current under G-protein modulation. 相似文献
4.
The purpose of the study was to determine whether Aβ1–42 and p-Tau181 cerebral spinal fluid (CSF) levels can predict progression from amnestic mild cognitive impairment (aMCI) to Alzheimer’s disease dementia (ADD) in a 3-year follow-up study. All participants were evaluated blindly by a behavioral neurologist and a neuropsychologist, and classified according to the Petersen criteria for aMCI and according to the Clinical Dementia Rating (CDR) scale. Individuals were also submitted to lumbar puncture at baseline. Levels of Aβ1–42 and p-Tau181 were measured by immunoenzymatic assay. Values were adjusted for age and sex. Thirty-one of 33 (93.9%) participants completed follow-up. Approximately 39% of aMCI individuals progressed to ADD. The relative risk of developing ADD in those with Aβ1–42 CSF levels lower than 618.5 pg/mL was 17.4 times higher than in those whose levels were higher than 618.5 pg/mL (P?=?0.003). p-Tau181 alone did not predict progression to ADD (P?=?0.101). The relative risk in those with a p-Tau181/Aβ1–42 ratio higher than 0.135 was 5.7 times greater (P?<?0.001). Aβ1–42 and p-Tau181 explained 40.1% of the verbal memory test subscore of the Consortium to Establish a Registry for Alzheimer’s Disease (ΔCERADs) variance (P?=?0.008). Aβ1–42 strongly predicted progression from aMCI to ADD. p-Tau181 alone, or its relation to Aβ1–42, was inferior than Aβ1–42 alone as a predictor of progression to ADD. 相似文献
5.
Qinggan Zeng Rongyong Man Yifeng Luo Ling Zeng Yushi Zhong Bingxun Lu Xiaofeng Wang 《Journal of molecular neuroscience : MN》2017,61(2):159-168
Using microarray analysis, we detected microRNA-124 (miR-124) to be abundantly expressed in the olfactory bulb (OB). miR-124 regulates adult neurogenesis in the subventricular zone (SVZ). However, much less is known about its role in newborn OB neurons. Here, using both gain-of-function and loss-of-function approaches, we demonstrate that brain-specific miR-124 affects dendritic morphogenesis and spine density in newborn OB neurons. Functional Annotation Clustering of miR-124 targets was enriched in “cell morphogenesis involved in neuron differentiation.” 相似文献
6.
The effects of co-administration of either the dopamine precursor, L-Dopa, or the directly-acting, mixed dopamine (DA) agonist, apomorphine, with the alpha-adrenoceptor agonists, clonidine and guanfacine, upon the motor activity of hypoactive L-Dopa-tolerant MPTP-treated C57 BL/6 mice were measured in four experiments. In each case, MPTP (2 x 40 mg/kg, s.c., separated by a 24-hr interval) was administered eight-to-ten weeks before behavioural testing. It was found that clonidine co-administered with L-Dopa (20 mg/kg) restored motor activity in a dose- and parameter-related manner: locomotion and total activity were restored by the 1 mg/kg dose, rearing behaviour by the 0.3 and 1 mg/kg doses. The restorative effects of clonidine (1 mg/kg), co-administered with L-Dopa, were antagonised completely by pretreatment with yohimbine (1 mg/kg), but not by prazosin (1 mg/kg). Guanfacine (1 mg/kg) co-administered with L-Dopa (20 mg/kg) restored locomotor, but not rearing, behaviour in L-Dopa-tolerant MPTP-treated mice. The antikinesic action of guanfacine was antagonised completely by yohimbine (1 mg/kg), but not prazosin (1 mg/kg). Clonidine (1 or 3 mg/kg) co-administered with apomorphine (0.1, 0.3, 1.0 or 3.0 mg/kg), directly-acting DA agonist, did not restore motor behaviour in the hypokinesic L-Dopa-tolerant MPTP-treated mice. Nor did apomorphine, by itself, affect the motor activity of these animals. Neurochemical analysis indicated marked DA, DOPAC and HVA depletions in the striatum, and to a much lesser extent in the frontal cortex, of MPTP-treated mice. The synergistic antiparkinsonian action of clonidine with L-Dopa, but not apomorphine, in hypokinetic MPTP mice for the restoration of responding to a suprathreshold dose of L-Dopa, to which "wearing-off" had been induced previously, is discussed. 相似文献
7.
Many currently prescribed antiepileptic drugs (AEDs) act via voltage-gated sodium channels, through effects on γ-aminobutyric
acid-mediated inhibition, or via voltage-gated calcium channels. Some newer AEDs do not act via these traditional mechanisms.
The molecular targets for several of these nontraditional AEDs have been defined using cellular electrophysiology and molecular
approaches. Here, we describe three of these targets: α2δ, auxiliary subunits of voltage-gated calcium channels through which the gabapentinoids gabapentin and pregabalin exert their
anticonvulsant and analgesic actions; SV2A, a ubiquitous synaptic vesicle glycoprotein that may prepare vesicles for fusion
and serves as the target for levetiracetam and its analog brivaracetam (which is currently in late-stage clinical development);
and Kv7/KCNQ/M potassium channels that mediate the M-current, which acts a brake on repetitive firing and burst generation and serves
as the target for the investigational AEDs retigabine and ICA-105665. Functionally, all of the new targets modulate neurotransmitter
output at synapses, focusing attention on presynaptic terminals as critical sites of action for AEDs. 相似文献
8.
The changes in the mRNA levels of α2A and α2C adrenoceptors were investigated in unilateral 6-OHDA-lesioned rat model of Parkinson’s disease and l-DOPA-induced dyskinesia using in situ hybridization. In the untreated 6-OHDA-lesioned rats, α2A expression was elevated in the locus coeruleus (160 ± 8% and 142 ± 8% in lesioned and unlesioned sides compared to the comparable
side in sham-operated rats). Following long-term (21 days, twice daily) treatment with l-DOPA (25 mg/kg l-DOPA methyl ester plus benserazide 6.25 mg/kg) in 6-OHDA-lesioned rats, levels of α2A adrenoceptor mRNA in the locus coeruleus were decreased, compared to the 6-OHDA-lesioned rats, returning to the levels of
α2A mRNA in the sham-operated rats. α2A adrenoceptor expression was not changed in other brain regions in any treatment group. There was no change in α2C expression in the rostral or caudal striatum in which the highest density of α2C mRNA is present. In conclusion, the data presented in this study demonstrate an increase in α2A adrenoceptor mRNA in the locus coeruleus in the 6-OHDA-lesioned rat model of Parkinson’s disease. In addition, the data show
that repeated treatment with l-DOPA in 6-OHDA-lesioned rats, which induces dyskinesia, restores α2A mRNA levels. These changes of α2A mRNA expression, observed in the locus coeruleus, might be of importance to basal ganglia transmission and motor function. 相似文献
9.
10.
ProThyrotropin-releasing hormone (proTRH) is a prohormone widely distributed in many areas of the brain. After biosynthesis,
proTRH is subjected to post-translational processing to generate TRH and seven non-TRH peptides. Among these non-TRH sequences,
we found previously that preproTRH178–199 could regulate the secretion of prolactin in suckled rats by their pups. Dopamine (DA), the main regulator of prolactin secretion,
is produced in dopaminergic tyrosine hydroxylase (TH)-positive neurons in the hypothalamic arcuate nucleus (ARC). In this
study we investigated whether prolactin release during the estrous sexual cycle is regulated by prepro TRH178–199 through its effecton DA neurons of the ARC. We observed that biotinylated prepro TRH178–199 bound to neurons in the ARC; this was higher during proestrus than during diestrus. Binding of preproTRH178–199 to DA neurons was seen only during proestrus in the ARC. Using primary neuronal hypothalamic cultures we found that preproTRH178–199peptide decreased TH levels in a dose-responsive manner, whereas intra-ARC administration of preproTRH178–199 induced a 20-fold increase in plasma prolactin levels. Together, these results suggest a potential role for preproTRH178–199 in regulating dopaminergic neurons involved in the inhibition of pituitary prolactin release. 相似文献
11.
Strokes promote immunosuppression, partially from increased sympathetic activity. Altering sympathetic drive with β-blockers has variably been shown to improve stroke outcomes. This study adds to this literature using propensity score matching to limit confounding and by examining the effects of selective and non-selective β-blockers. Prospective data from acute ischemic stroke admissions at a single center from July 2010–June 2015 were analyzed. Outcomes included infection (urinary tract infection [UTI], pneumonia, or bacteremia), discharge modified Rankin Score (mRS), and in-hospital death. Any selective and non-selective β-blocker use during the first 3 days of admission were investigated with propensity score matching. A sensitivity analysis was also performed. This study included 1431 admissions. Any β-blocker use was associated with increased infections (16.4 vs. 10.7%, p = 0.030). Non-selective β-blocker use was associated with increased infections (18.9 vs. 9.7%, p = 0.005) and UTIs (13.0 vs. 5.5%, p = 0.009). Selective β-blocker use was not associated with infection. There were no associations between β-blocker use and in-hospital death or discharge mRS. In the sensitivity analysis, the association between non-selective β-blocker use and urinary tract infections persisted (12.5 vs. 4.2%, p = 0.044). No associations with death or mRS were found. Early β-blocker use after ischemic stroke may increase the risk of infection but did not change disability or mortality risk. The mechanism may be mediated by β2-adrenergic receptor antagonism given the different effects seen with selective versus non-selective β-blocker use. 相似文献
12.
13.
Platelet phospholipase A<Subscript>2</Subscript> activity in Alzheimer’s disease and mild cognitive impairment 总被引:1,自引:0,他引:1
Gattaz WF Forlenza OV Talib LL Barbosa NR Bottino CM 《Journal of neural transmission (Vienna, Austria : 1996)》2004,111(5):591-601
Summary. Phospholipase A2 (PLA2) controls the metabolism of phospholipids in cell membranes. In the brain, PLA2 influences the processing of the amyloid precursor protein (APP) and thus the production of the amyloid-beta peptides (A), which are the major components of the senile plaques in Alzheimers disease (AD). Reduced PLA2 activity has been reported in brain and in platelets of AD patients. In the present study we investigated PLA2 activity in platelets from 21 AD patients as compared to 17 healthy elderly controls and 11 individuals with mild cognitive impairment (MCI). Subjects were cognitively assessed by the Mini-Mental State Examination (MMSE) and the CAMDEX schedule. Platelet PLA2 activity was determined by radio-enzymatic assay, which mainly detected a calcium-independent form of the enzyme present also in the brain (iPLA2). PLA2 activity was significantly lower in AD than in controls (p<0.001). Mean PLA2 activity in MCI individuals was between the values of AD patients and controls, with a subgroup showing PLA as low as the lowest AD patients, but the differences from MCI were not significant from AD and control groups. Lower PLA2 activity was significantly correlated with a worse cognitive performance both at the MMSE (p=0.001) and the cognitive sub-scale of the CAMDEX inventory (p=0.002). Our data replicate previous findings of reduced platelet PLA2 activity in AD. Both reduced PLA2 activity and the correlation with impaired cognition were also reported in brain tissue of AD patients, suggesting thus that the present determinations in platelets may be related to a reduction in the brain. In the brain the inhibition of PLA2 inhibits the physiological secretion of the APP, a mechanism that increases A formation. Further longitudinal studies should investigate whether those MCI individuals with the lowest PLA2 values in platelets would be at a higher risk to develop AD during a longitudinal follow up. 相似文献
14.
Xue Fu Meiling Ke Weihua Yu Xia Wang Qian Xiao Min Gu Yang Lü 《Journal of molecular neuroscience : MN》2018,65(2):179-189
Inhibition of endocytosis in an Alzheimer’s disease (AD) model has been shown to be able to prevent amyloid β (Aβ)-induced damage and to exert a beneficial effect in treating AD. Adaptor-associated kinase 1 (AAK1), which binds to the adaptor protein complex 2 (AP-2), regulates the process of clathrin-mediated endocytosis. However, how AAK1 expression varies over the course of AD is unknown. In this study, we investigated AAK1 levels in AD model mice over time. Aβ1–42 was used to establish a mouse AD model, and the Morris water maze test was used to characterize the time course of Aβ1–42-induced cognition changes. ELISA was used to determine AAK1 levels in plasma and Aβ1–42 levels in brain tissues. Subsequently, the protein or gene levels of AAK1, AP-2, and Rab5 (an early endosome marker) were tested in each group. The cognitive function of Aβ1–42-induced mice was significantly declined compared to control group, and the deficits reached a peak on day 14, but partly recovered on day 30. Moreover, the level of Aβ1–42 detected with ELISA was highest on day 14, but reduced on day 30, paralleling the cognitive changes in the mice in our study. AAK1, AP-2, and Rab5 expression showed the same periodic variation as the changes in cognition. Thus, periodic variation in AAK1 expression is closely correlated to the decline in cognition, and AAK1 might be a suitable indicator for Alzheimer’s disease. 相似文献
15.
Kazue?Kikuchi-Utsumi Mami?Ishizaka Nobuko?Matsumura Masahiko?Watabe Koji?Aoyama Nobuyuki?Sasakawa Toshio?Nakaki
Methamphetamine (METH) is a psychostimulant that damages nigrostriatal dopaminergic terminals, primarily by enhancing dopamine and glutamate release. α1-adrenergic receptor (AR) subtype involved in METH-induced neurotoxicity in rats was investigated using selective α1-AR antagonists. METH neurotoxicity was evaluated by (1) measuring body temperature; (2) determining tyrosine hydroxylase (TH) immunoreactivity levels; (3) examining levels of dopamine and its metabolites; and (4) assessing glial fibrillary acidic protein (GFAP) and microglial immunoreactivity in the striatum. METH caused a decrease in dopamine and TH levels and induced hyperthermia which is an exacerbating factor of METH neurotoxicity. Concurrently, METH increased GFAP expression and the number of activated microglia. Pretreatment with prazosin, a nonselective α1-AR antagonist, completely abolished METH-induced decrease in both dopamine and TH and caused a partial reduction in hyperthermia. Prazosin also prevented METH-induced increase in both GFAP expression and the number of activated microglia. In vivo microdialysis analysis revealed that prazosin, however, does not alter the METH-induced dopamine release in the striatum. The neuroprotective effects of prazosin could be mimicked by a selective α1D antagonist, BMY 7378, but not by selective α1A or α1B antagonists. These results suggest that the α1D-AR is involved in METH-induced hyperthermia and neurotoxicity in rats. 相似文献
16.
Steffensen LH Jørgensen L Straume B Mellgren SI Kampman MT 《Journal of neurology》2011,258(9):1624-1631
Multiple sclerosis (MS) is a possible cause of secondary osteoporosis. In this phase II trial we assessed whether a weekly
dose of 20,000 IU vitamin D3 prevents bone loss in ambulatory persons with MS age 18–50 years. ClinicalTrials.gov ID NCT00785473. All patients managed
at the University Hospital of North Norway who fulfilled the main inclusion criteria were invited to participate in this double-blinded
trial. Participants were randomised to receive 20,000 IU vitamin D3 or placebo once a week and 500 mg calcium daily for 96 weeks. The primary outcome was the effect of the intervention on percentage
change in bone mineral density (BMD) at the hip, the spine, and the ultradistal radius over the study period. Of 71 participants
randomised, 68 completed. Mean serum 25-hydroxyvitamin D [25(OH)D] levels in the intervention group increased from 55 nmol/L
at baseline to 123 nmol/L at week 96. After 96 weeks, percentage change in BMD did not differ between groups at any site.
BMD decreased at the hip, by 1.4% in the placebo group (95% CI −2.3 to −0.4, SD 2.7, p = 0.006) and by 0.7% in the treatment group (−1.6 to 0.2, 2.7, p = 0.118), difference 0.7% (−1.9 to 0.7, p = 0.332). Findings were not altered by adjustment for sex or serum 25(OH)D. Supplementation with 20,000 IU vitamin D3 a week did not prevent bone loss in this small population. Larger studies are warranted to assess the effect of vitamin D
on bone health in persons with MS. 相似文献
17.
Díaz-Cabiale Z Parrado C Fuxe K Agnati L Narváez JA 《Journal of neural transmission (Vienna, Austria : 1996)》2007,114(1):115-125
Summary. The nucleus tractus solitarii (NTS) is a key nucleus in central cardiovascular control. In this mechanism it is well known
the role of the α2-adrenoreceptors for the modulation of the autonomic pathways. Moreover a number of neuropeptides described in the NTS, including
Neuropeptide Y (NPY), Galanin (GAL) and Angiotensin II (Ang II), have different roles in regulating the cardiovascular function
within this nucleus. We show in this review several data which help to understand how these neuropeptides (NPY, GAL and Ang
II) could modulate the cardiovascular responses mediated through α2-adrenoreceptors in the NTS. Also we show for the first time the interactions between neuropeptides in the brain, specifically
the interactions between NPY, GAL, and Ang II, and its functional relevance for central cardiovascular regulation. These data
strength the role of neuropeptides on central autonomic control and provide some evidences to understand the neurochemical
mechanisms involved in the cardiovascular responses from the NTS. 相似文献
18.
Gerlach M Bartoszyk GD Riederer P Dean O van den Buuse M 《Journal of neural transmission (Vienna, Austria : 1996)》2011,118(12):1733-1742
Sarizotan, a 5-HT1A agonist with additional affinity for D3 and D4 receptors, has been demonstrated to have anti-dyskinetic effects. The mechanism by which these effects occur is not clear.
Using unilateral 6-hydroxydopamine-lesioned rats that received chronic intraperitoneal (ip) administration of l-3,4-dihydroxyphenylalanine (l-DOPA) we investigated the involvement of D3 and 5-HT1A receptors in the effects of sarizotan on contraversive circling and abnormal involuntary movements (AIMs). Before sensitization
by chronic l-DOPA treatment (12.5 with 3.25 mg/kg benserazide ip, twice daily for 21 days), no effect of the selective D3 agonist, PD128907 (1 or 3 mg/kg ip), or the selective D3 antagonist, GR103691 (0.5 or 1.5 mg/kg ip), was observed. Treatment with sarizotan (1 or 5 mg/kg ip) dose-dependently inhibited
the l-DOPA-induced contraversive turning and AIMs. In co-treatment with the 5-HT1A antagonist, WAY100635 (1 mg/kg ip), sarizotan failed to affect this behaviour, confirming the prominent 5-HT1A receptor-mediated mechanism of action. In the presence of PD128907 (3 mg/kg ip), the effects of sarizotan on contraversive
turning, locomotive dyskinesia and axial dystonia, but not on orolingual and forelimb dyskinesia, were blocked. On its own,
PD128907 had no effect on the behavioural effects of l-DOPA except that it tended to reduce orolingual and forelimb dyskinesia. GR103691 had no effect on its own or in combination
with sarizotan. These data identify an involvement of D3 receptors in the action of sarizotan on some, but not all l-DOPA-induced motor side effects. This selective involvement is in contrast to the more general involvement of 5-HT1A receptors in the anti-dyskinetic effects of sarizotan. 相似文献
19.
Prolonged spin–spin relaxation times in tumour tissue have been observed since some of the earliest nuclear magnetic resonance investigations of the brain. Over the last three decades, numerous studies have sought to characterize tumour morphology and malignancy using quantitative assessment of T 2 relaxation times, although attempts to categorize and differentiate tumours have had limited success. However, previous work must be interpreted with caution as relaxation data were typically acquired using a variety of multiple echo sequences with a range of echoes and T 2 decay curves and were frequently fit with monoexponential analysis. We defined the distribution of T 2 components in three different human brain tumours (glioblastoma, oligodendroglioma, meningioma) using a multi-echo sequence with a greater number of echoes and a longer acquisition window than previously used (48 echoes, data collection out to 1120 ms) with no a priori assumptions about the number of exponential components contributing to the T 2 decay. T 2 relaxation times were increased in tumour tissue and each tumour showed a distinct T 2 distribution profile. Tumours have complex and unique compartmentalization characteristics. Quantitative assessment of T 2 relaxation in brain cancer may be useful in evaluating different grades of brain tumours on the basis of their T 2 distribution profile, and has the potential to be a non-invasive diagnostic tool which may also be useful in monitoring therapy. Further study with a larger sample size and varying grades of tumours is warranted. 相似文献
20.
Přikrylová Vranová H Mareš J Hluštík P Nevrlý M Stejskal D Zapletalová J Obereigneru R Kaňovský P 《Journal of neural transmission (Vienna, Austria : 1996)》2012,119(3):353-362
Parkinson’s disease (PD) is a neurodegenerative disorder with highly heterogeneous clinical manifestations. This fact has
prompted many attempts to divide PD patients into clinical subgroups. This could lead to a better recognition of pathogenesis,
improving targeted treatment and the prognosis of PD patients. The aim of the present study was to obtain cerebrospinal fluid
(CSF) samples in PD patients and to search for a relationship between neurodegenerative CSF markers (tau protein, beta-amyloid1-42 and index tau protein/beta-amyloid1-42) and the clinical subtypes. PD patients were divided into three subgroups: early disease onset (EDO), tremor-dominant PD
(TD-PD), and non-tremor dominant PD (NT-PD) according to the previously published classification. Neurodegenerative markers
in the CSF were assessed in these three groups of patients suffering from PD (EDO-17, TD-15, NT-16 patients) and in a control
group (CG) of 19 patients suffering from non-degenerative neurological diseases and 18 patients with Alzheimer’s disease (AD).
The NT-PD patients were found to have significantly higher levels of CSF tau protein and index tau/beta than the control subjects
and other Parkinsonian subgroups, but no significant differences in these markers were found between AD and NT-PD patients.
In the context of more rapid clinical progression and more pronounced neuropathological changes in the NT-PD patient group,
our results corroborate the opinion that CSF level of tau protein may be regarded as a potential laboratory marker of the
presence and severity of neurodegeneration. 相似文献