[ ISSN : 2573-6728 ]
Obsessive Compulsive Disorder; BDNF; Val66Met polymorphism; Susceptibility; Neurotrophin
Brain-Derived Neurotrophic Factor (BDNF) is required for neuron growth and maintenance. Single nucleotide polymorphisms (SNP) are reported in BDNF gene, which reduces proteins activity, Val66Met polymorphism is very well studied and reported as a risk factor for psychiatric diseases. Numerous case-control studies have evaluated the role BDNF Val 66Met (dbSNP: rs6265;196G>A) polymorphism in OCD susceptibility and provided ambiguous findings, hence present meta-analysis was designed to get an exact association between BDNF Val66Met polymorphism and OCD risk. A total of 14 case - control articles were identified through PubMed, Google Scholar, Science Direct and Springer link databases search, up to July 11, 2024. Odds ratios (ORs) with 95% con¬fidence intervals (CIs) were used as association measure. All statistical analyses were done by MetaDiSc (version 1.4).
Fourteen case-control studies involving 2,765 OCD cases and 5,585 controls were included in present meta-analysis. The results showed that the BDNF Val66Met polymorphism was not associated with OCD risk (allele contrast odds ratio ORAvsG = 0.96, 95% CI= 0.82-1.12, p= 0.000; homozygote ORAAvsGG = = 0.79, 95%CI= 0.59-1.06, p= 0.0058; dominant model ORAA+GAvsGG = 0.96, 95%CI= 0.86-1. 06, p= 0.17). In conclusion, the BDNF Val66Met polymorphism was not related to increased OCD susceptibility.
Obsessive compulsive disorder (OCD) is a mental health condition characterized by repetitive intrusive thoughts, images and impulses (obsessions) and repetitive behaviours (compulsions). It is a leading cause of mental disability worldwide [1], with a lifetime prevalence of 1.3 - 2.3% [2,3]. In addition to being associated with significant functional impairment in daily living and quality of life [4,5], OCD has been associated with neurocognitive deficits, as measured using neuropsychological assessment. The average age of onset is around 19 years old. It affects men and women equally, but the onset in males is earlier than in females.
Genome-wide and twin studies reported higher involvement of hereditary factors in OCD [1, 6]. Published studies have reported numerous OCD candidates genes including COMT, SERT, SLC1A1, DLGAP1, PTPRD, NRXN1, HTR2A, CTTNBP2, REEP3 and BDNF [1,6]. BDNF (Brain-Derived Neurotrophic Factor) is a crucial protein belonging to the neurotrophin family, which supports the survival, development, neural plasticity and function of neurons [7 -10]. BDNF helps in the generation of new neurons from neural stem cells in hippocampus. BDNF has been reported to affect the synthesis of neurotransmitters and expression of their receptors. It regulates moods and reduced /altered BDNF expression involved in the pathophysiology of various psychiatric and neurodegenerative disorders, including depression, anxiety, schizophrenia, and bipolar disorder. It is reported very well that antidepressants and other medications up regulate BDNF expression.
BDNF gene is located at chromosome 11p14.1, spans about 70 kb and has a complex structure, it consists of 11 exons (I–IX, plus Vh and VIIIh), the coding sequence resides only in exon 9, and all upstream exons encode promoters, regulating regional and cell-type-specific expression (Figure 1). The gene contains multiple promoters that allow for tissue-specific and activity-dependent expression of BDNF. BDNF expression is tuned in response to various intrinsic and extrinsic stimuli. Exon IX, encodes precursor-BDNF protein (pre-pro-BDNF; ~ 27 kDa) in endoplasmic reticulum [11].
Several single nucleotide polymorphism are reported in BDNF genes include rs6265, rs11030101, rs12291186, rs7934165, rs11030104, rs1519480, rs8192466, rs539177035, and rs551669106 [12-14]. Val66Met polymorphism is located in exon 9 in which G is substituted by A at 196 position (G196A), resulting in substitution of amino acid valine with methionine at 66th codon (Val66Met). Val66Met alteration affects the activity-dependent secretion of BDNF, which is important for neuronal development, synaptic plasticity, neurogenesis and cognitive function. Val/Val genotype is generally associated with normal BDNF function. Met carriers (Val/Met or Met/Met) is often exhibit reduced activity-dependent BDNF secretion. Imaging and autopsy studies have reported functional and structural alterations in met allele carriers especially in hippocampus and prefrontal cortex regions. BDNF levels are associated with cognitive functions, mood regulation, and overall brain health. Decreased BDNF levels have been linked to cognitive decline and mood disorders such as depression. After knowing clinical implications of Val66Met polymorphism, authors designed and performed metaanalysis of case control studies to shed light on exact association between Val66Met polymorphism and OCD susceptibility.
Eligible studies were identified by searching Pubmed, Springer link, Science Direct and Google Scholar databases up to July 11, 2024. The following search terms were used: “Brain Derived Neurotrophic Factor” or “BDNF”, and “Val158Met” in combination with “Obsessive compulsive disorder”, or “OCD”. Inclusion criteria for selection of studies were: (i) study should be published, (ii) case control approach was used by authors, and (iii) allele number/ genotypes numbers were reported in the study to calculate OR with 95%CI. Studies were excluded from the meta-analysis if: (i) studies based on pedigree data (ii) study was review, letter to editor or editorial and (iii) other genes variants are analysed in OCD patients.
The following data was extracted from each included study: (i) first author’s family name, (ii) country name and ethnicity, (iii) number of cases and controls and (iv) number of alleles and/or number of genotypes in both cases and controls for recalculation of ORs with 95% CI (Confidence Interval).
Pooled OR with corresponding 95% confidence Interval (CI) was used as association measure to assess the risk between Met allele and OCD susceptibility. A pooled OR was estimated on the basis of the individual ORs. OR was estimated either by using fixed effects [15], or random effects [16], model depending upon heterogeneity (I2 ). If I2 > 50% then random effect model was used. Pooled ORs were calculated using different genetic models, viz.: (i) allelic contrast model (A vs.G), (ii) homozygote model (AA vs. GG), (iii) dominant model (AA+ GA vs. GG), and (iv) recessive model (AA vs. GA+ GG) [17]. Method of Guo et al. [18], was adopted for quality score assessment. The quality scores ranged from 0 to 10 and studies with score <5 was defined as low quality, and studies with score ≥7 was defined as high quality. Meta-analysis was undertaken by free program MetaDiSc (version 1.4), developed by Zamora et al. [19]. All P values are two-tailed with a significance level at 0.05
After applying inclusion and exclusion criteria, total 13 studies were found to be eligible for present meta-analysis [1,20-31] (Table 1). In one study [22], authors analysed cases from two countries viz.- South Africa and The Netherland, so both samples were included separately in the meta-analysis. Hence, total studies included in current metaanalysis was fourteen. In included meta-analysis, samples with several countries/population were analysed like-America [20], Brazil [24], China [23, 27, 29], India [1], Japan [31], Mexico [28], South Africa [21,26], The Netherlands [22], and Turkey [25] (Table 1).
Table 1: Details of included fourteen studies in present meta-analysis
In total 14 included studies, the number of cases were 2765 and number of controls was 5585. GG, GA and AA genotypes number in cases are 1434, 1028, and 303, respectively. In controls, GG, GA, AA genotypes number were 2571, 2320 and 694, respectively (Table 1) (Figure 3). In cases and controls T allele frequencies were 29.55 % and 33.2%. Meta-analysis of samples of 14 studies, adopting allele contrast model (A vs. G) showed no significant association with both fixed and random effects models. Higher heterogeneity was observed (I2 = 71.5%), so random effect model was adopted. The random effect pooled ORAvs G was 0.96 (95% CI= 0.82-1.12; p= 0.000) and Cochran Q was 45.55 (df = 13; p=0.000). The tau squared is 0.0596 (Figure 4)
Figure 1 : BDNF gene structure showing Val66Met polymorphism .
Figure 2 : Flow diagram of article selection
Figure 3 : Bar diagram showing number of GG, GA and AA genotypes in case and control samples of included studies.
Figure 4 : Allele contrast forest plot adopting random effect model
Association between OCD and Val66Met polymorphism using homozygote (AA vs GG; homozygote model), was also not found (ORAAvs GG= 0.79; 95%CI= 0.59-1.06; p= 0.0058; Cochran Q=29.35), higher heterogeneity (I2 =55.7%) was present, so random effect was adopted (Figure 5). Results of meta-analysis using dominant models (ORAA+GAvs GG= 0.96; 95%CI= 0.86-1. 06; p= 0.17; Cochran Q=15.56; I2 =25.9) did not show significant association. Egger’s test were performed to estimate the risk of publication bias. Except allele contrast and homozygote model, publication bias was absent (G vs. A: P Egger’s test= 0.03; AG vs. AA: P Egger’s test= 0.29; GG vs. AA: P Egger’s test P= 0.03; Dominant model GG+AG vs. AA: P Egger’s test= 0.06; Recessive model GG vs. AG+GG: P Egger’s test= 0.05) It is very well established fact that BDNF is required for overall brain/neuron health and mutation in this gene affects brain activities and modulates moods, hence is reported a risk factor for psychiatric as well as neurodegenerative disorders including anxiety disorders [32], obsessive-compulsive disorder [33], depression [34, 35], bipolar disorder[34], schizophrenia [34,36], eating disorders [37], as well as alcohol and substance-use disorders [38], Alzheimer’s disease [39], Parkinson’s disease [40], and multiple sclerosis [41].
Figure 5 : Homozygote contrast forest plot adopting random effect model.
The results of present metaanalysis suggested that Met (A) allele is not risk for OCD, instead A/met allele protects against OCD During past thirty years, meta-analysis is used for summarization and revalidation of results of individual case –control studies. Metaanalysis are continuously published to evaluate disease risk of small effect genes like- tuberculosis [42], Cleft lip and Palate [43], NTD [44], Down syndrome [45-47], Obsessive compulsive disorder [48], depression [49,50], schizophrenia [51], bipolar disorder [52,53], autism [54], alcohol dependence [55-57], migraine [58], epilepsy [59], Alzheimer’s disease [60], male infertility [61], osteoporosis [62], recurrent pregnancy loss [63], uterine leiomyoma [64], lung cancer [65], digestive tract cancer [66], breast cancer risk [67,68], esophageal cancer [69], prostate cancer [70- 72], endometrial cancer [73], ovary cancer [74], and MTRR [75].
Present meta-analysis had few limitations also, that should also be acknowledged- (i) case sample size is small, (ii) used crude ORs without adjustment, (iii) single BDNF polymorphism is considered and (iv) gene environment interaction is not considered. In conclusion, the present meta-analysis reported no association between the BDNF Val66Met polymorphism and OCD risk. Met allele is not a risk for OCD, instead plays a protective role. However, due to presence of higher heterogeneity, results should be cautiously interpreted. In future, well-designed meta-analysis considering cofounding factors and gene-environment interactions should be performed to confirm exact associations in different ethnic populations.
Authors acknowledge the funding received from UP higher Education Council (Centre of Excellence-9/2022/447/ seventy-4-2022-04(17)/2021; Date 15-03-2022).
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The F-wave is a result of α-motor neurons backfiring following an antidromic invasion of propagated impulses across the axon hillock.
Suzuki T*
Atypical hand preference may be more common in Adults Who Stutter (AWS). One implication is that stuttering may be a manifestation of a more general dysfunction in motor organization and planning. This study was designed to determine whether AWS have atypical motor cortical anatomy compared to controls, and whether there are group differences in handedness that correlate with anatomical measures. Volumetric MRI was used to measure the anterior bank of the Central Sulcus (CS) and Motor Knob (MK), a structure that corresponds precisely to the motor hand representation, in Adults Who Stutter (AWS) and fluent, matched controls divided into three groups (right-handed and left-handed men, right-handed women). There was an interaction between fluency group and handedness-sex group (p=0.024) with reduced CS volume in right-handed men who stutter (p=0.001). For MK volume there was an interaction with the right MK larger in the left-handed male controls, and the left MK larger in the left-handed AWS (p=0.024). AWS and controls did not differ in hand preference score or finger tapping rate. There was a relationship between CS asymmetry and finger-tapping laterality (p=0.042) with a faster right-hand tapping speed associated with a larger left CS and vice-versa. When controls were examined independently, there were no correlations between finger-tapping laterality and anatomical asymmetry; there was a correlation in the AWS (r= 0.642; p= 0.007). Left hander AWS tapped faster with the right hand and had a larger left CS (atypical). One subgroup of right handed AWS (atypical) tapped faster with the left hand and had a larger right CS. Another subgroup of right handed AWS (typical) tapped faster with the right hand and had a larger left CS. These results show that handedness may systematically influence cortical motor representations in AWS. Further study is warranted in a larger sample of adults and in children who stutter.
Foundas LA¹*, Baucom CC², Knaus TA³, and Corey DM⁴
Objective: To study the ischemic stroke subtypes and risk factors in 100 patients observed at Jordan University Hospital (JUH) over a one-year-period, and to compare the results with another 100 age-and –sex matched controls as well as with studies from other Arab countries.
Methods: One hundred patients with first-ever ischemic stroke admitted to JUH over a one-year period (between January 2013 to January 2014) were studied.
Results: There were 62 males and 38 females (M/F ratio=1. 6), with a mean age of 66 years (range 22-90 years), the majority (80/100) between the age 51-80 years. The most common stroke subtype was lacunar infarcts (36 patients). Fourty-two out of 51 patients had intracranial atherosclerosis. The most common risk factor was hypertension (85%) followed by hyperlipidemia (71%) and diabetes mellitus (65%).
Conclusion: In accordance with other Arab studies and controls, hypertension was the predominant risk factor but lacunar infarcts were more common than in most reports from other Arab countries . This shows the importance of appropriate management of hypertension to reduce the incidence of stroke in Jordan.
Bahou Y*, Ajour M, and Jaber M
Background: Language ability is one of the strongest predictors of prognosis and developmental course in Autism Spectrum Disorder (ASD). A range of language abilities occur in ASD and although many have delays in language it remains unclear why some children’s language continues to lag, while others do not. Abnormal anatomy and function of language-related regions has been found in ASD, however, how these differences relate to language development over time is undetermined.
Methods: This study examined longitudinal changes in language functions in children with ASD and investigated whether cortical language region anatomy was related to these changes in language. Eighteen boys with ASD, 2-8 years old were evaluated (Time 1) and re-examined about 3.5 years later (Time 2) at ages 7-10. MRIs were collected at Time 2 to evaluate gray matter volume of anterior (Pars Triangularis, PTR; pars opercularis, POP) and posterior (Planum Temporale, PT; Posterior Superior Temporal Gyrus, pSTG) language regions and the microstructure of the arcuate fasciculus.
Results: Eleven boys had relative decline in language functions (decline group) and 7 boys had no relative change in language (no change group). The no change group had larger PT and right PTR volume relative to the decline group. In addition, the right PTR was correlated with the language change score, with larger right PTR associated with less language decline. There was a trend for non-right-handers to have more language decline than right-handers.
Conclusions: Results suggest differences in cortical language anatomy may play a role in language development, with further studies warranted.
Tracey A Knaus¹˒²*, Jodi Kamps³˒⁴, and Anne L Foundas⁵
From the observation of different F-wave waveforms, we introduce a new method of differentiating these waveforms, by assigning each with an “F-wave waveform value”, which can be used in the clinic to evaluate the effects of rehabilitation. F-wave waveform values were determined by creating a window from minimum onset latency to maximum onset latency in measurable waveforms. We then calculated the correlation coefficient of each waveform, using Microsoft Excel, and identified F-waves as those with a correlation coefficient of greater than 0.9 or equal to 1.0. The number of different F-wave waveforms types was determined from the number of identified waveforms. We applied F-wave waveform values to evaluate neurophysiological change and the effects of rehabilitation following hemiplegia. In the future, F-wave waveform values should be considered as an important tool when assessing the effects of rehabilitation on impaired neurological responses.
Toshiaki Suzuki¹˒²*, Yoshibumi Bunno¹˒², Makiko Tani¹˒², Chieko Onigata², Yuuki Fukumoto¹, Marina Todo², Hirofumi Watanabe³, Toshihiro Ohnuma¹˒²˒³, and Naoko Komatsu³
The consumption of nutrients containing phenolic compounds has been reported due to the benefits they produce on human health. Therefore, the objective of this study was to investigate the antioxidant and neuroprotective effect of the administration of organic (OGJ) and conventional (CGJ) white grape juices from Niagara variety on the oxidative stress in cerebral cortex, hippocampus and cerebellum after the treatment with carbon tetrachloride (CCl4 ) as well as on some biochemical parameters in serum of rats. Adult male rats (~300g; n=6-8/group) were orally treated (gavage) with 7μL/g of OGJ, CGJ or water, for a period of 14 days. On the 15th day it was administered CCl4 (3.0mL/kg). After 4h the animals were euthanized and the cerebral cortex, hippocampus and cerebellum were dissected and used for the analysis of oxidative stress parameters. We observed that CCl4 enhanced lipid peroxidation (TBARS) and protein damage (carbonyl), reduced the nonenzymatic antioxidants defenses (sulfhydryl), and changed the activity of the enzymatic antioxidants defenses catalase (CAT), Superoxide Dismutase (SOD) in the brain of rats. CCl4 also enhanced glucose, Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST) and Gamma-Glutamyl (GGT) and decreased total cholesterol and High-Density Lipoprotein (HDL) in serum of rats. CGJ and OGJ were able to prevent or ameliorate most of these alterations. Consequently, regular intake of white grape juice could be considered as an adjuvant in the therapy of oxidative damages, revealing a possible antioxidant and neuroprotective agent.
Clarice M. Peripolli, Tatiane Gabardo, Fernanda de Souza Machado, Mariane Wohlenberg, Juliana D.O. Lima, Alice S. Oliveira, Marina Rocha Frusciante, Niara da Silva Medeiros, Sheila Pereira Feijó, Filipe V.V. Nascimento, Caroline Dani, and Cláudia Funchal
It has been over 27 years since Blum & Noble discovered the first association of the DRD2 A1 allele in severe alcoholism, suggesting reward as the real phenotype, not alcoholism. This has been acknowledged by an explosion of research in the arena of Psychiatric Genetics. To date, a PubMed search listed 6,839 studies (5-15- 17). The A1 allele has been associated with substance use disorders other than alcoholism, including cocaine, nicotine dependence, polysubstance abuse and many Reward Deficiency Syndrome (RDS) behaviors substance and non-substance related. Certainly following extensive controversy, the emerging evidence suggests that the DRD2 is a reinforcement or reward gene. In fact, it could represent one of the most prominent single-gene determinants of susceptibility to severe substance abuse/reward deficiency. While, however, the environment through epigenetic impact and other genes, when combined, still play the larger role, targeting the DRD2 gene through the novel genetic rewriting of the DNA code at the mRNA level may hold the greatest promise to date for potentially “curing” the RDS phenotype.
Kenneth Blum¹⁻⁹˒¹²*, Mark S Gold²˒¹⁵, Lloyd G Mitchell¹⁰˒¹¹, Kareem W Washington¹⁰, David Baron², Panayotis K Thanos¹³, Bruce Steinberg¹⁴, Edward J Modestino¹⁴, Lyle Fried⁷, and Rajendra D Badgaiyan¹²
Background: Pharmacological treatment for AD and depression are unfortunately few and of limited efficacy to cure the disease.
Objectives: To assess the combined effects of rivastigmine and citalopram on Alzheimer’s Disease.
Methods: Longitudinal clinical prospective study with 1278 AD patients on rivastigmine 9,5mg/patch and citalopram 20-40 mg/day over 48 months was assessed on the basis of NINCDS-ADRDA, MMSE, DSM-IV, FRSSD, GDS, HRS-D and follow up of the patients.
Results: Four years after the baseline assessment, there were no significant differences in MMSE, Geriatric depression scale and Hamilton rating scale for depression between patients treated with rivastigmine alone or combined rivastigmine with citalopram with or without depression (p>0.05). Functional Rating Scale for symptoms of dementia, Activities of Daily Living of patients with AD and depression treated with rivastigmine was significantly worse than patients treated with rivastigmine and no depression (p=0.027).
Conclusions: The combination of rivastigmine and citalopram had no better results than rivastigmine alone in patients with AD.
Magda Tsolaki*, Krishna Prasad Pathak, Eleni Verikouki, Chaido Zchou Messini, Tara Gaire, and Paschalis Devranis
Anxiety is one of the most clinically significant psychiatric syndromes in Parkinson’s Disease (PD). It is estimated to affect up to 50% of individuals with PD and is associated with higher levels of dependency and poorer quality of life. Although it is common, it remains widely under recognised by patients, carers and clinicians, and has not been extensively studied [1]. Therefore, in spite of its significant impact, the symptomatology, chronology, and neurobiology of anxiety in PD are not well understood.
Recently, anxiety in PD has been associated with increases in motor fluctuations and gait disturbances including freezing. Freezing of gait (FOG) is the temporary inability to walk and is one of the most debilitating symptoms of PD. It is associated with an increase in falls, injuries and dependency. The associations with motor symptoms have significant consequences for the quality of life of people living with PD. This review summarizes the most recent data on the epidemiology, associated features and possible mechanisms underlying anxiety in PD.
Perri Carlson-Hawke¹˒²*, Belinda Brown², and Simon Hammond¹
Ramsay hunt syndrome arises from a constellation of cranial nerve involvement, commonly facial nerve and trigeminal nerve along with erythematous rash in ear/ over the eye secondary to Varicella Zoster Virus (VZV) reactivation. We describe an unusual presentation of herpes zoster in an immunocompetent individual with several brainstem nuclei involvement mimicking a brain stem stroke. This presentation is termed as brain stem radiculitis.
Sushma R Yerram*