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1.
Over the last decades, increasing knowledge about the genetic architecture of Parkinson’s disease has provided novel insights
into the pathogenesis of the disorder, generating hypotheses for further research. Characterizing the role of SNCA, encoding the α-synuclein protein, has been a particularly important aspect of this development. The identification of SNCA as the first gene implicated in monogenic parkinsonism led to the recognition of α-synuclein as a key protein in the pathogenesis
and a major component of pathological hallmark lesions. An association between common variants in SNCA and risk of sporadic Parkinson’s disease has been established through numerous studies. We review our current understanding
of SNCA variability contributing to Parkinson’s disease, highlighting the characterization of functionally relevant susceptibility
alleles as a major future challenge. We argue that new strategies will be needed to pinpoint the variants that are ultimately
responsible for the signals detected in association studies, where targeted resequencing may represent an attractive initial
approach. 相似文献
2.
Neda Shahmohammadibeni Simin Rahimi-Aliabadi Javad Jamshidi Babak Emamalizadeh Hossein Ali Shahmohammadibeni Alireza Zare Bidoki Haleh Akhavan-Niaki Hajar Eftekhari Shokoufeh Abdollahi Mahmoud Shekari Khaniani Mahnaz Shahmohammadibeni Atena Fazeli Marzieh Motallebi Shaghayegh Taghavi Azadeh Ahmadifard Amir Ehtesham Shafiei Zarneh Monavvar Andarva Tahereh Dadkhah Ehteram Khademi Elham Alehabib Mahnoosh Rahimi Abbas Tafakhori Minoo Atakhorrami Hossein Darvish 《Neurological sciences》2016,37(5):731-736
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder. Both genetic and environmental factors are involved in the etiology of the disease. Many studies have revealed the susceptibility genes and variations for PD which need further confirmation. Here we evaluated the association of variations in SNCA, HUSEYO and CSMD1 genes with PD. A case–control study was conducted with 489 PD patients and 489 healthy controls. DNA was extracted from peripheral blood of all subjects and rs356220 and rs11931074 in SNCA, rs2338971 in HUSEYO and rs12681349 in CSMD1 were genotyped using PCR–RFLP method. The genotypes and allele frequencies were significantly different between case and control groups for rs356220, rs11931074 and rs2338971 but not for rs12681349. We provided further evidence that rs356220 is associated with increased risk of PD supporting previous studies in Caucasian-based and Japanese populations. The association of rs11931074 with decreased risk of PD was also significant. This study revealed the first evidence of the association of rs2338971 with increased risk of PD in the Iranian population. Nevertheless, these findings need further validation via more replication studies. 相似文献
3.
Claudia Funke Juergen Tomiuk Olaf Riess Daniela Berg Anne S. Soehn 《Journal of neural transmission (Vienna, Austria : 1996)》2009,116(7):853-859
Parkinson’s disease (PD) is characterized by the loss of dopaminergic neurons and the presence of intracytoplasmic inclusions
(Lewy bodies). Iron, which is elevated in the substantia nigra (SN) of PD patients, seems to be of pivotal importance, because
of its capacity to enhance the amplification of reactive-oxygen species. Therefore, it is tempting that the iron-releasing
key enzyme in heme catabolism, heme oxygenase-1 (HO-1), may represent a candidate for a genetic susceptibility to PD. In the current study, we examined a (GT)n fragment length
polymorphism in the promoter region, as well as three coding SNPs in the HO-1 gene in order to assess if certain genotypes are associated with PD. Furthermore, peripheral blood expression levels of HO-1 in PD patients and healthy probands were compared. However, our analyses did not reveal a significant association of these
genetic markers in the HO-1 gene with an increased susceptibility to PD. 相似文献
4.
Lamei Yuan Zhi Song Xiong Deng Zhijian Yang Yan Yang Yi Guo Hongwei Lu Hao Deng 《神经科学通报》2017,33(5):510-514
Parkinson’s disease (PD) is the second most common neurodegenerative disorder and has an elusive etiology. It is likely multifactorial, and genetic defects contribute to its pathogenesis. At least 25 genetic loci and 20 monogenic genes have been identified in monogenic PD. Recessive F-box protein 7 gene (FBXO7) mutations reportedly cause hereditary parkinsonism. To explore the roles of four paralogs (FBXO2, FBXO6, FBXO12, and FBXO41) in PD development, their variants (rs9614, rs28924120, rs6442117, and rs61733550, respectively) were analyzed in 502 Han Chinese patients with PD and 556 age, gender, and ethnicity-matched normal participants in mainland China. Statistically significant differences in genotypic and allelic frequencies were detected only in the FBXO2 variant rs9614 (P = 0.001 and 0.023, respectively; odds ratio 0.819, 95% confidence interval 0.690–0.973) between patients and controls. These results suggest that the FBXO2 variant rs9614 C allele may decrease the PD risk in mainland Han Chinese and may be a biomarker for PD. 相似文献
5.
Quadri M Cossu G Saddi V Simons EJ Murgia D Melis M Ticca A Oostra BA Bonifati V 《Neurogenetics》2011,12(3):203-209
Mutations in the TARDBP gene are a cause of autosomal dominant amyotrophic lateral sclerosis (ALS) and of frontotemporal lobar degeneration (FTLD),
but they have not been found so far in patients with Parkinson’s disease (PD). A founder TARDBP mutation (p.Ala382Thr) was recently identified as the cause of ~30% of ALS cases in Sardinia, a Mediterranean genetic isolate.
We studied 327 consecutive Sardinian patients with clinically diagnosed PD (88 familial, 239 sporadic) and 578 Sardinian controls.
One family with FTLD and parkinsonism was also included. The p.Ala382Thr heterozygous mutation was detected in eight unrelated
PD patients (2.5%). The three patients from the FTLD/parkinsonism family also carried this mutation. Within the control group,
there were three heterozygous mutation carriers. During follow-up, one of these individuals developed motoneuron disease and
another, a rapidly progressive dementia; the third remains healthy at the age of 79 but two close relatives developed motoneuron
disease and dementia. The eight PD patients carrying the p.Ala382Thr mutation had all sporadic disease presentation. Their
average onset age was 70.0 years (SD 9.4, range 51–79), which is later but not significantly different from that of the patients
who did not carry this mutation. In conclusion, we expand the clinical spectrum associated with TARDBP mutations to FTLD with parkinsonism without motoneuron disease and to clinically definite PD. The TDP-43 protein might be
directly involved in a broader neurodegenerative spectrum, including not only motoneuron disease and FTLD but also PD. 相似文献
6.
Qicong Chen Biyu Liang Ziyou Wang Xiaoguang Cheng Yifeng Huang Yong Liu Zunnan Huang 《Neurological sciences》2016,37(8):1209-1220
We preformed this meta-analysis to investigate the influence of ABCA1 (ATP-binding cassette sub-family A member 1) rs2422493 (C-477T), rs1800977 (C-14T), rs2066718 (V771M), and PTGS2 (Prostaglandin-endoperoxide synthase 2) rs20417 (G-765C) polymorphisms on the risk of Alzheimer’s disease (AD). Seventeen eligible case–control studies were acquired from PubMed, Embase, Alzgene, Chinese National Knowledge Infrastructure and Wanfang databases. The pooled odds ratios (ORs) with 95 % confidence intervals (95 % CI) were calculated to evaluate the association under five genetic models. Combined data indicated that ABCA1 rs2422493 polymorphism was statistically significant associated with increasing AD risk in three genetic models (allelic T vs C: OR = 1.12, 95 % CI: 1.01–1.24; homozygous TT vs CC: OR = 1.26, 95 % CI: 1.03–1.55; and recessive TT vs TC + CC: OR = 1.33, 95 % CI: 1.12–1.58) while no association was found between two other ABCA1 polymorphisms and AD susceptibility. Nevertheless, a further risk-stratification analysis showed that ApoE-ε4 carriers with any ABCA1 polymorphism suffered a much higher probability to be AD patients. Meanwhile, PTGS2 rs20417 polymorphism was linked to decreasing AD risk with a P < 0.0001 in five genetic models (e.g., allelic C vs G: OR = 0.59, 95 % CI: 0.50–0.70; homozygous CC vs GG: OR = 0.31, 95 % CI: 0.18–0.52; and heterozygous CG vs GG: OR = 0.64, 95 % CI: 0.52–0.78). In summary, our meta-analysis results showed that ABCA1 rs2422493 polymorphism was a risk factor for AD while PTGS2 rs20417 variant showed a protective effect on AD risk. In addition, ABCA1 rs2066718 and rs1800977 polymorphisms might not contribute to AD susceptibility in general population, but they should play a role on AD development when interacted with ApoE-ε4. 相似文献
7.
Goris A Williams-Gray CH Foltynie T Brown J Maranian M Walton A Compston DA Barker RA Sawcer SJ 《Journal of neurology》2007,254(7):846-848
Given the known roles of TGFbeta2 in both regulating the immune system and promoting the survival of dopaminergic neurons, it is feasible that genetic variations in TGFB2 might play an aetiological role in neurological diseases such as Multiple Sclerosis (MS) and Parkinson's disease (PD). Hence we performed an indirect association analysis of TGFB2 using 8 haplotype-tagging SNPs in a population of 937 MS patients, 538 PD cases and 2022 controls. We found no evidence for association with susceptibility or progression of MS, but have demonstrated a trend towards association of the 5' region of the gene with susceptibility to PD. Further analysis of TGFB2 is warranted in other PD cohorts. 相似文献
8.
Previous studies have claimed the association of rs12720208 polymorphism in the fibroblast growth factor 20 (FGF20) gene with the increased risk of Parkinson’s disease (PD), but results from the published data were controversial. The aim of our present meta-analysis was to estimate the overall association between FGF20 rs12720208 polymorphism and the risk of PD. Case–control studies with sufficient data evaluating the association between rs12720208 C/T polymorphism and PD susceptibility were systematically identified in PubMed, OVID, SinoMed, Chinese National Knowledge Infrastructure (CNKI) up to July 10, 2015. A total of 3402 PD patients and 3739 controls from seven case–control studies were collected for this meta-analysis. The pooled odds ratio (OR) with its 95 % confidence interval (CI) was calculated to assess the genetic association between FGF20 rs12720208 polymorphism and the risk of PD. In this study, no enough proof was found to prove the association in any genetic models with random-effects model (CT+TT vs. CC: OR = 1.147, 95 % CI: 0.883–1.489, P = 0.304; TT vs. CC+CT: OR = 1.754, 95 % CI: 0.878–3.505, P = 0.112; T vs. C: OR = 1.169, 95 % CI = 0.919–1.487, P = 0.204; TT+CC vs. CT: OR = 0.906, 95 % CI = 0.694–1.182, P = 0.466). Our results suggest that there is no sufficient evidence to support the association between rs12720208 polymorphism and PD risk. Studies with larger sample size across diverse populations and subgroup analyses are necessary in the future. 相似文献
9.
Jun-Ying Li Jin-hong Zhang Nan-Nan Li Ling Wang Zhong-Jiao Lu Lan Cheng Xiao-Yi Sun Rong Peng 《Neurological sciences》2017,38(2):343-347
Recent several meta-analyses and certain case–control studies suggested that the Ras-like without CAAX 2 (RIT2) rs12456492 increased the risk of Parkinson’s disease (PD) in Asian and Caucasian populations. However, as so far, the association between RIT2 rs12456492 and PD is still controversial. We investigated genetic association of RIT2 rs12456492 with PD susceptibility in a Han Chinese population of 1747 ethnic Han Chinese subjects comprising 884 PD patients and 863 healthy controls. The minor allele frequency (MAF) of G at the RIT2 rs12456492 was not significantly different between the cases and the controls. Furthermore, no significant differences were observed in genotype distribution between PD patients and healthy controls for the RIT2 rs12456492, even after being stratified by age at onset and gender. In addition, we found that no significant differences were detected in the clinical manifestations for gender, age at onset, and onset symptoms between PD patients with AG + GG genotypes and those with AA genotypes. Our study from the mainland China demonstrates that RIT2 rs12456492 do not increase the risk of developing PD. Therefore, more replication studies in additional Chinese population and other cohorts are warranted to further clarify the role of RIT2 rs12456492 in PD susceptibility. 相似文献
10.
Yun Yan Su Xiao Dong Zhang U. Joseph Schoepf Akos Varga-Szemes Andrew Stubenrauch Xue Liang Li Juan Zheng Gang Zheng Xiang Kong Qiang Xu Shou Ju Wang Rong Feng Qi Guang Ming Lu Long Jiang Zhang 《Brain imaging and behavior》2017,11(3):818-828
In this study, we used resting-state functional magnetic resonance imaging to explore the genetic effects of amyloid precursor protein (APP) or presenilins mutation and apolipoprotein E (APOE) ε4 on the default-mode network (DMN) in cognitively intact young adults (24.1 ± 2.5 years). Both the APP or presenilin-1/2 group and the APOE ε4 group had significantly lower DMN functional connectivity (FC) in the some brain regions like precuneus/middle cingulate cortices (PCu/MCC) than controls (AlphaSim corrected, P < 0.05). Only a lower FC tendency was demonstrated (control < APOE ε4 < APP or presenilin-1/2 group). Moreover, lower FC in PCu/MCC is correlated with some neuropsychological assessments such as similarity test in APOE ε4 group. These findings indicate that DMN FC alteration in APP or presenilin-1/2 or APOE ε4 subjects is prior to the occurrence of neurological alterations and clinical symptoms, and DMN FC might be a valuable biomarker to detect genetic risk in the preclinical stage. 相似文献
11.
Nian Xiong Nuomin Li Eden Martin Jinlong Yu Jie Li Jing Liu David Yue-Wei Lee Ole Isacson Jeffery Vance Hong Qing Tao Wang Zhicheng Lin 《Neurotherapeutics》2016,13(3):623-634
Vesicular monoamine transporter 2 (VMAT2) is responsible for sequestering cytosolically toxic dopamine into intracellular secretory vesicles. Animal genetic studies have suggested that reduced VMAT2 activity contributes to the genetic etiology of Parkinson’s disease (PD), but this role has not been established in humans. Based on human genetic association and meta-analysis, we first confirm the human VMAT2 (hVMAT2 or SLC18A2) promoter as a risk factor for PD in both family and unrelated US white people: marker rs363324 at –11.5 kb in the hVMAT2 promoter is reproducibly associated with PD in a cohort of nuclear families (p = 0.04506 in early-onset PD) and 3 unrelated US white people (meta-analysis p = 0.01879). In SH-SY5Y cells, low activity-associated hVMAT2 promoter confers high methylpiperidinopyrazole iodide cytotoxicity, which is likely attributed to functional polymorphisms bound by nuclear proteins. Interestingly, treatments with the dopamine neuron-protecting agent puerarin upregulates the promoter activity in a haplotype- and cell line-dependent manner. These pharmacogenetic findings suggest that hVMAT2 could be a risk factor and imply it as a target of genetic medications for PD. 相似文献
12.
Anoushe Zhand Arezou Sayad Soudeh Ghafouri-Fard Shahram Arsang-Jang Mehrdokht Mazdeh Mohammad Taheri 《Neurological sciences》2018,39(11):1945-1953
Epilepsy is a brain disorder with a global prevalence of 1%. It has been attributed to genetics and environmental factors. Despite efforts to identify the molecular pathology of epilepsy, the underlying mechanism is not understood yet. This study was carried out to compare GRIN2B, BDNF, and IL-1β gene expressions in 50 patients suffering from generalized epilepsy with tonic-colonic seizures and 50 age- and sex-matched healthy subjects using TaqMan Real-time PCR. Our results demonstrated significant upregulation of these genes in people with epilepsy compared with healthy subjects. We also found a positive correlation between GRIN2B and BDNF expression (r2=0.4619, p?<?0.0001), BDNF and IL-1β expression (r2?=?0.515, p?<?0.0001), and GRIN2B and IL-1β gene expressions (r2?=?0.666, p?<?0.0001) which implies the possibility to estimate the expression level of these genes by assessment of expression of one of them. Considering the results of the previous animal studies which showed upregulation of these genes in brain tissues of epileptic animals, the expression levels of GRIN2B, BDNF, and IL-1β in blood samples might be related to their expression in brain samples. Future studies are needed to assess the role of these genes in the pathogenesis of epilepsy and evaluate whether altered expression of these genes along with imaging methods can facilitate subtyping the epilepsy. 相似文献
13.
Phenotype analysis in patients with early onset Parkinson’s disease with and without <Emphasis Type="Italic">parkin</Emphasis> mutations 总被引:1,自引:0,他引:1
The data regarding whether parkin genotype attributes phenotypic variation are conflicting. Since the incidence of parkin mutations is very low in patients with an age at onset (AAO) of >40 years, previous studies have unfairly compared phenotypes
of two early onset Parkinson’s disease (EOPD) groups with different AAOs. Thus, we compared the clinical features between
patients with and without parkin mutations in EOPD with an AAO of ≤40 years. Of the 124 patients with EOPD with an AAO of ≤40 years who were recruited and
screened for parkin mutations, 84 completed assessments for comparison of the phenotype according to parkin genotype. Fourteen of the 84 subjects carried two parkin mutations; 6, a single mutation; and 64, no mutations. Patients with two mutations had significantly younger AAOs, longer
duration of PD, and more common family history than patients without parkin mutations. Otherwise, motor and nonmotor symptoms did not differ between them. Subgroup analysis of EOPD with an AAO of ≤35 years
revealed similar results. Phenotype of EOPD may depend on early AAOs rather than presence of parkin mutations. 相似文献
14.
Aihua Yang Chenxuan Wang Baomin Song Wendi Zhang Yuanyuan Guo Rong Yang Guangjun Nie Yanlian Yang Chen Wang 《神经科学通报》2017,33(4):405-412
Accumulation and aggregation of β-amyloid (Aβ) peptides result in neuronal death, leading to cognitive dysfunction in Alzheimer’s disease. The self-assembled Aβ molecules form various intermediate aggregates including oligomers that are more toxic to neurons than the mature aggregates, including fibrils. Thus, one strategy to alleviate Aβ toxicity is to facilitate the conversion of Aβ intermediates to larger aggregates such as fibrils. In this study, we designed a peptide named A3 that significantly enhanced the formation of amorphous aggregates of Aβ by accelerating the aggregation kinetics. Thioflavin T fluorescence experiments revealed an accelerated aggregation of Aβ monomers, accompanying reduced Aβ cytotoxicity. Transgenic Caenorhabditis elegans over-expressing amyloid precursor protein exhibited paralysis due to the accumulation of Aβ oligomers, and this phenotype was attenuated by feeding the animals with A3 peptide. These findings suggest that the Aβ aggregation-promotion effect can potentially be useful for developing strategies to reduce Aβ toxicity. 相似文献
15.
Guiyou Liu Tao Wang Rui Tian Yang Hu Zhifa Han Pingping Wang Wenyang Zhou Peng Ren Jian Zong Shuilin Jin Qinghua Jiang 《Journal of molecular neuroscience : MN》2018,66(1):37-43
Genetic association studies have identified significant association between the GAB2 rs2373115 variant and Alzheimer’s disease (AD). However, it is unknown whether rs2373115 affects the regulation of nearby genes. Here, we evaluate the potential effect of rs2373115 on gene expression using multiple eQTL (expression quantitative trait loci) datasets from human brain tissues from the Mayo Clinic brain expression genome-wide association study (eGWAS), the UK Brain Expression Consortium (UKBEC), the Genotype-Tissue Expression (GTEx) project, and the Brain xQTL Serve. Our findings indicate that the rs2373115 C allele is associated with increased NARS2 expression, and both reduced and increased GAB2 expression in human tissues. Using a large-scale AD case-control expression dataset, we found increased GAB2 expression and reduced NARS2 expression in AD cases compared with controls. We believe that our findings provide important information regarding the rs2373115 variant and expression of nearby genes with respect to AD risk. 相似文献
16.
Oxidative stress has been proposed to be an important factor in the pathogenesis of Alzheimer’s disease (AD) and contributed
to β-amyloid (Aβ) generation. Interaction between oxidative stress and neuro-inflammation leads to Aβ generation. AD is associated with an
increase in blood–brain barrier (BBB) permeability due to tight junction involvement. Oxidative stress decreases the expression
of low-density lipoprotein receptor-related protein 1 and up-regulates receptor for advanced glycation end products in BBB
and increases the BBB permeability, which could potentially lead to increased deposition of Aβ within AD brain. Apoptosis takes place in the pathogenesis of AD, and oxidative stress contributes to apoptosis through both
extrinsic pathway and intrinsic pathway. Oxidative stress-induced apoptosis may be a potential factor to Aβ generation. Aβ generation requires two sequential cleavages of APP, with the two proteolytic enzymes: β-secretase and γ-secretase. Oxidative damage up-regulates Aβ via inducing activity of β- and γ-secretases. In this review, we will focus on the mechanism and pathway that oxidative stress contributes to Aβ generation. 相似文献
17.
Avner Thaler Elissa Ash Ziv Gan-Or Avi Orr-Urtreger Nir Giladi 《Journal of neural transmission (Vienna, Austria : 1996)》2009,116(11):1473-1482
Mutations in the leucine rich repeat kinase 2 gene (LRRK2) are recognized as the most common cause of genetic Parkinsonism to date. The G2019S mutation has been implicated as an important
determinant of Parkinson’s disease (PD) in both Ashkenazi Jewish and North African Arab populations with carrier frequency
of 29.7% among familial and 6% in sporadic Ashkenazi Jewish PD cases. PD patients with the G2019S mutation display similar
clinical characteristics to patients with sporadic PD. While the function of the LRRK2 protein has yet to be fully determined, its distribution coincides with brain areas most affected by PD. The G2019S mutation
is believed to be responsible for up-regulation of LRRK2 kinase activity, which may ultimately play a role in neuronal loss. The utility of LRRK2 G2019S screening in family members of Ashkenazi PD patients is discussed. LRRK2 G2019S mutation carriers without PD may be an ideal population for the study of possible neuroprotective strategies as they
become available, and for furthering the understanding of the pathogenesis and long-term clinical outcomes of the disease. 相似文献
18.
The distribution of cerebrovascular amyloid in Alzheimer’s disease varies with <Emphasis Type="Italic">ApoE</Emphasis> genotype 总被引:1,自引:0,他引:1
Trembath D Ervin JF Broom L Szymanski M Welsh-Bohmer K Pieper C Hulette CM 《Acta neuropathologica》2007,113(1):23-31
We performed a comparative study to assess cerebral amyloid angiopathy and ApoE genotype in cases of Alzheimer’s disease (AD). Ten ApoE 3,3 and ten ApoE 4,4 AD brains, as well as ten normal control brains, were selected after matching for age, sex, and duration of disease. Sections of middle frontal and inferior parietal cortex including white matter sections were stained with an antibody against amyloid beta (Aβ), and extensive analysis of arteriolar Aβ deposition was performed using digital image analysis. Quantification of the staining revealed a larger cross-section of arteriolar walls occupied by Aβ in ApoE 4,4 and ApoE 3,3 AD subjects compared to controls. Our results show Aβ deposition in gray matter and white matter arterioles was predominantly found in ApoE 4,4 brains and, overall, Aβ deposition was greatest in these cases. This observation implies that there is greater vascular amyloid deposition (particularly in the white matter arterioles) in ApoE 4,4 AD individuals compared to ApoE 3,3 AD. These observations may give insight into the etiology behind the increased risk for AD associated with the ApoE-ε4 allele and the pathogenesis of vascular Aβ deposition.This study was supported by the National Institutes of Health NIA P50 AG05128 and P30 AG028377. 相似文献
19.
Abramsson A Landgren S Zetterberg M Seibt Palmer M Minthon L Gustafson DR Skoog I Blennow K Zetterberg H 《Neuromolecular medicine》2011,13(2):160-166
Aggregation of amyloid-beta is one of the major characteristics in brains of patients with Alzheimer’s disease (AD). Although
several mechanisms behind the formation of such aggregates have been suggested the regulatory factors are still unknown. The
present study aimed at investigating the association of lysyl oxidase-like 1 (LOXL1) polymorphisms with AD diagnosis and cerebrospinal fluid biomarkers (CSF) for the disease. Proteins of the lysyl oxidase (LOX) family are involved in cross-linking extracellular matrix proteins to insoluble fibers and have been associated with neurodegenerative
diseases including AD. Genetic polymorphisms in LOXL1 (rs1048661, rs3825942, and rs2165241) have been linked to exfoliation syndrome and exfoliation glaucoma, conditions that
have shown association with AD. The polymorphisms were genotyped by Taqman allelic discrimination in a study sample including
AD patients (n = 318) and controls (n = 575). In a subgroup of the population, the polymorphisms were analyzed in relation to APOE ε4 genotype and to CSF (T-tau, P-tau, and Aβ1–42). No evidence for associations of these polymorphisms with risk for AD or any of the studied CSF biomarkers measured was
found. These results do not support LOXL1 as being a major risk gene for AD. 相似文献
20.
Gennaro Pagano Tayyabah Yousaf Marios Politis 《Current neurology and neuroscience reports》2017,17(11):90