Journal of systems and integrative neuroscience最新文献

{"title":"Cardiovascular diseases and Alzheimer's disease: A potential relationship","authors":"E. Koutsouraki, D. Michmizos","doi":"10.15761/jsin.1000208","DOIUrl":"https://doi.org/10.15761/jsin.1000208","url":null,"abstract":"The study of the relationship between cardiovascular diseases (CVDs) and Alzheimer’s disease (AD) can be complicated. The diagnostic criteria of AD usually exclude patients with any clinical CVD (the combination of CVD and dementia leading more strongly towards a diagnosis of multi-infarction dementia rather than in AD). Nevertheless, there is strong evidence supporting the notion that CVDs contributes at least to the onset of AD, as demonstrated by numerous autopsy studies. The incidence of microvascular ischemic episodes has been found to strongly correlate with Dementia. Nevertheless, it is not clear whether this association is due to the fact that they share common risk factors or if the CVDs are directly or indirectly involved in the pathogenesis leading to AD. Understanding the etiology of one of these diseases can lead to understanding the onset, progression and treatment of the other. *Correspondence to: Effrosyni Koutsouraki, 1stDepartment of Neurology, Medical School, Aristotle University, AHEPA Hospital, St. Kyriakidi 1, Thessaloniki, Greece, E-mail: efrosink@gmail.com","PeriodicalId":87318,"journal":{"name":"Journal of systems and integrative neuroscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67485054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The benefits of genetic addiction risk score (GARS™) and pro-dopamine regulation in combating suicide in the American Indian population.","authors":"Kenneth Blum, David Siwicki, David Baron, Edward J Modestino, Rajendra D Badgaiyan","doi":"10.15761/JSIN.1000195","DOIUrl":"10.15761/JSIN.1000195","url":null,"abstract":"<p><p>It is well-known that Native Americans (NA) clinically present with a very high rate of alcoholism and other drugs of abuse. It is also known that NA also display a very high rate of suicide compared to other ethnic groups. Furthermore, individuals with various psychiatric disorders (e.g., depression) also have higher rates of suicide that are frequently alcohol related. Males are as much as four times more likely to die from suicide than females. Studies comparing Native to other populations within the same geographic regions in North America divulged, almost universally, that alcohol involvement is higher among Native suicides than among the local, non-Native people. Unfortunately, suicide is the eighth leading cause of death in the U.S. and is the third cause of death in those ages 15-24. With these disappointing statistics, we are hereby proposing that because of such a high genetic risk as supported by the work of Barr and Kidd showing that NA carriers the DRD2 A1 allele at the rate of 86%, compared to a highly screened reward deficiency free control of only 3%. It seems reasonable that early identification, especially in children, be tested with the Genetic Addiction Risk Score (GARS) and concomitantly be offered the precision pro-dopamine regulator (KB220PAM), one that matches their unique brain polymorphisms involving serotonergic, endorphinergic, glutaminergic, gabaergic and dopaminergic pathways among others. We believe that using the Precision Addiction Management (PAM) platform at an early age may be prophylactic, while in adults PAM may reduce substance craving affecting tertiary treatment and even relapse and mortality prevention.</p>","PeriodicalId":87318,"journal":{"name":"Journal of systems and integrative neuroscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6816273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49325128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Our evolved unique pleasure circuit makes humans different from apes: Reconsideration of data derived from animal studies.","authors":"Kenneth Blum,&nbsp;Marjorie Gondré-Lewis,&nbsp;Bruce Steinberg,&nbsp;Igor Elman,&nbsp;David Baron,&nbsp;Edward J Modestino,&nbsp;Rajendra D Badgaiyan,&nbsp;Mark S Gold","doi":"10.15761/JSIN.1000191","DOIUrl":"https://doi.org/10.15761/JSIN.1000191","url":null,"abstract":"<p><p>The brain regions tied to pleasure can be triggered by engaging in sex, eating tasty food, watching a movie, accomplishments at school and athletics, consuming drugs, and noble efforts to help the community, the country, and the world. It is noteworthy that research suggests that the latter type of satisfaction, supporting the community, may result in the most substantial positive effects on our immune system. However, these pathways for these effects are not understood. Berridge and Kringelbach have suggested that pleasure is mediated by well-developed mesocorticolimbic circuitry and serves adaptive functions. In affective disorders, anhedonia (lack of pleasure) or dysphoria (negative affect) can result from a breakdown of that hedonic system. Most importantly, human neuroimaging investigations indicate that surprisingly similar circuitry is activated by quite diverse pleasures, suggesting a common neural pathway shared by all rewarding stimuli and behaviors. Over many years the controversy of dopamine involvement in pleasure/reward has led to confusion in terms, such as trying to separate motivation from pure pleasure (i.e., wanting versus liking). We take the position that animal studies cannot provide real clinical information that is described by self-reports in humans. On November 23^rd, 2017, evidence for our concerns was revealed. A brain system involved in everything from addiction to autism appears to have evolved differently in humans than in apes, as reported by a large research team in the journal <i>Science</i>. To reiterate, the new findings by Sousa et al., also suggest the importance of not over-relying on rodent and even non-human primate studies. Extrapolations, when it comes to the concept of pleasure, dopamine, and reinforcement, are not supported by these data. Human experience and study are now much more critical and important. Extrapolations from non-humans to humans may be more fiction than fact. While this statement is bold it should not at all suggest that animal date is unimportant, that is not the case. It is extremely valuable in many aspects and we must encourage the development of animal models for disease. However, we must be cautious in our interpretation of results without leaping to conclusions that may be explained by follow-up human experiments and subsequent data. We are further proposing that in terms of overcoming a never -ending battle related to the current drug epidemic, the scientific community should realize that disturbing dopamine homeostasis by taking drugs or having a system compromised by genes or other epigenetic experiences, should be treated by alternative therapeutic modalities, expressed in this article as a realistic key goal. Application of genetic addiction risk (GARS™) testing and pro-dopamine regulation (KB220) should be considered along with other promising technologies including cognitive behavioral therapy, mind fullness, brain spotting and trauma therapy. Basic scien","PeriodicalId":87318,"journal":{"name":"Journal of systems and integrative neuroscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6446569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37130152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Would induction of dopamine homeostasis via coupling genetic addiction risk score (GARS®) and pro-dopamine regulation benefit benzodiazepine use disorder (BUD)?","authors":"Blum K, Gold Ms, Modestino Ej, Baron D, Boyett B, Siwicki D, Lott L, Podesta A, Roy Ak, Hauser M, Downs Bw, Badgaiyan Rd","doi":"10.15761/JSIN.1000196","DOIUrl":"https://doi.org/10.15761/JSIN.1000196","url":null,"abstract":"Prescriptions for Benzodiazepines (BZDs) have risen continually. According to national statistics, the combination of BZDs with opioids has increased since 1999. BZDs (sometimes called “benzos”) work to calm or sedate a person by raising the level of the inhibitory neurotransmitter GABA in the brain. In terms of neurochemistry, BZDs act at the GABAA receptors to inhibit excitatory neurons, reducing VTA glutaminergic drive to reduce dopamine release at the Nucleus accumbens. Benzodiazepine Use Disorder (BUD) is very difficult to treat, partly because BZDs are used to reduce anxiety which paradoxically induces hypodopaminergia. Considering this, we are proposing a paradigm shift. Instead of simply targeting chloride channel direct GABAA receptors for replacement or substitution therapy, we propose the induction of dopamine homeostasis. Our rationale is supported by the well-established notion that the root cause of drug and non-drug addictions (i.e. Reward Deficiency Syndrome [RDS]), at least in adults, involve dopaminergic dysfunction and heightened stress. This proposition involves coupling the Genetic Addiction Risk Score (GARS) with a subsequent polymorphic matched genetic customized Pro-Dopamine Regulator known as KB220ZPBM (Precision Behavioral Management). Induction of dopamine homeostasis will be clinically beneficial in attempts to combat BUD for at least three reasons: 1) During detoxification of alcoholism, the potential induction of dopamine regulation reduces the need for BZDs; 2) A major reason for BZD abuse is because people want to achieve stress reduction and subsequently, the potential induction of dopamine regulation acts as an anti-stress factor; and 3) BUD and OUD are known to reduce resting state functional connectivity, and as such, potential induction of dopamine regulation enhances resting state functional connectivity. Future randomized placebo-controlled studies will investigate this forward thinking proposed novel modality.","PeriodicalId":87318,"journal":{"name":"Journal of systems and integrative neuroscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49483033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vigilance behaviors and EEG activity in sustained attention may affect acute pain.","authors":"J H Chien, A Korzeniewska, A E Hillis, J H Kim, N Emerson, J D Greenspan, C M Campbell, T J Meeker, T M Markman, F A Lenz","doi":"10.15761/jsin.1000184","DOIUrl":"10.15761/jsin.1000184","url":null,"abstract":"<p><p>During Sustained Attention to stimuli across many modalities neural activity often decreases over time on task, while Errors in task performance increase (Vigilance Decrement). Sustained Attention to pain has rarely been investigated experimentally despite its clinical significance. We have employed a Sustained Attention protocol (Continuous Performance Task, CPT) in which the subject counts painful laser stimuli (targets) when they occur randomly in a prolonged train of nonpainful nontargets. We hypothesize that the magnitude of the poststimulus oscillatory power divided by baseline power (Event-Related Spectral Perturbation, ERSP - scalp EEG) over Frontoparietal structures will decrease at all frequencies with time on task, while Beta ERSP (14-30Hz) will be correlated with Error Rates in performance of the CPT. During the CPT with a painful target ERSP was found in four separate Windows, as defined by both their frequency band and the time after the stimulus. A Vigilance Decrement was found which confirms that Sustained Attention to pain was produced by this CPT. In addition, Error Rates was correlated inversely with laser energy, and with ratings of pain unpleasantness and salience. Error Rates also were related directly to the Beta ERSP Window at scalp EEG electrodes over the central sulcus. Over time on task, the ERSP magnitude decreased in Alpha (8-14Hz) Window, was unchanged in early and late Delta/Theta Windows (0-8Hz), and increased in the Beta Window. The increase in Beta ERSP and a decrease in the Alpha ERSP occurred at the same EEG electrode over the parietal lobe to a significant degree across subjects. Overall, Beta activity increases with time on task, and with higher Error Rates as in the case of other modalities. In the case of pain increased Errors correspond to misidentification of painful and nonpainful stimuli and so modulate the sensation of pain under the influence of Sustained Attention.</p>","PeriodicalId":87318,"journal":{"name":"Journal of systems and integrative neuroscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8294460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39210903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"\"Dopamine homeostasis\" requires balanced polypharmacy: Issue with destructive, powerful dopamine agents to combat America's drug epidemic.","authors":"Kenneth Blum,&nbsp;Edward J Modestino,&nbsp;Marjorie Gondré-Lewis,&nbsp;B William Downs,&nbsp;David Baron,&nbsp;Bruce Steinberg,&nbsp;David Siwicki,&nbsp;John Giordano,&nbsp;Thomas McLaughlin,&nbsp;Jennifer Neary,&nbsp;Mary Hauser,&nbsp;Lyle Fried,&nbsp;Rajendra D Badgaiyan","doi":"10.15761/JSIN.1000183","DOIUrl":"https://doi.org/10.15761/JSIN.1000183","url":null,"abstract":"<p><p>The well-researched pro-dopamine regulator KB220 and variants result in increased functional connectivity in both animal and human brains, and prolonged neuroplasticity (brain cell repair) having been observed in rodents. Moreover, in addition to increased functional connectivity, recent studies show that KB220Z increases overall brain connectivity volume, enhances neuronal dopamine firing, and eliminates lucid dreams in humans over a prolonged period. An unprecedented number of clinical studies validating this patented nutrigenomic technology in re-balancing brain chemistry and optimizing dopamine sensitivity and function have been published. On another note, it is sad that unsuspecting consumers could be deceived and endangered by false promises of knock-off marketers with look- and- sound-alike products. Products containing ingredients having potential dangers (i.e., combinations of potent D2 agonists including L-Dopa and L-Theanine) threaten the credibility and reputation of validated, authentic, and ethical products. We encourage clinicians and neuroscientists to continue to embrace the concept of \"dopamine homeostasis\" and search for safe, effective, validated and authentic means to achieve a lifetime of recovery, instead of reverting to anti-dopaminergic agents doomed to fail in the war against the devastating drug epidemic, or promoting powerful D2 agonists that compromise needed balance.</p>","PeriodicalId":87318,"journal":{"name":"Journal of systems and integrative neuroscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6128292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36476613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of residential dual diagnosis treatment on alcohol abuse.","authors":"Stephen J Schoenthaler,&nbsp;Kenneth Blum,&nbsp;Lyle Fried,&nbsp;Marlene Oscar-Berman,&nbsp;John Giordano,&nbsp;Edward J Modestino,&nbsp;Rajendra Badgaiyan","doi":"10.15761/JSIN.1000169","DOIUrl":"https://doi.org/10.15761/JSIN.1000169","url":null,"abstract":"<p><p>This multi-center study of dual diagnosis (DD) programs involved 804 residential patients with co-occurring alcohol and mental health disorders. The Addiction Severity Index was administered at admission and at one, six, and 12 months after discharge. Repeated measures analysis showed the intoxication rate per month stabilized between months six and 12 with 68% still in remission and an 88% mean reduction from baseline (F = 519, p < .005). A comparison between patients with and without weekly relapse produced significant differences in hospitalization (odds ratio 11.3:1; 95% C.I., 5.5 to 23.2). Eight ANCOVAs used mean intoxication days per month after discharge as the outcome variable, pre-admission intoxication days per month as a covariate, and eight variables associated with relapse (e.g. depression) as factors. Patients with these factors at admission did not have significantly higher intoxication rates after discharge than patients without them. This suggests that these DD programs successfully integrated treatment of both disorders and explained their effectiveness. Co-occurring DSM IV mood disorders such as anxiety and depression as well as drug abuse involving opioids or cocaine fell between 66 and 95% at months one, six, and twelve.</p>","PeriodicalId":87318,"journal":{"name":"Journal of systems and integrative neuroscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5576155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35470182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of IL-6, IL-1β and TNF-α production in monocytes isolated from multiple sclerosis patients treated with disease modifying drugs.","authors":"Sarah E Fiedler,&nbsp;Joshua D George,&nbsp;Haley N Love,&nbsp;Edward Kim,&nbsp;Rebecca Spain,&nbsp;Dennis Bourdette,&nbsp;Sonemany Salinthone","doi":"10.15761/JSIN.1000166","DOIUrl":"https://doi.org/10.15761/JSIN.1000166","url":null,"abstract":"<p><strong>Objective and design: </strong>The etiology of multiple sclerosis (MS) is unknown, but blood derived monocytes/macrophages are believed to be involved in the pathogenesis through phagocytosis of myelin and production of inflammatory mediators. The objective of this study is to examine inflammatory cytokines that are present at elevated levels in active MS lesions to determine whether there are differences between classically stimulated monocytes isolated from healthy control (HC) and relapsing-remitting MS (RRMS) subjects taking disease modifying drugs (DMDs), including dimethyl fumarate (DMF).</p><p><strong>Subjects: </strong>Thirty-nine veterans of the US Armed Forces were enrolled, 21 health controls (HC), and 18 with relapsing-remitting MS (RRMS), all taking DMDs.</p><p><strong>Methods: </strong>Use ELISAs to measure production of IL-6, IL-1β and TNF-α by LPS-stimulated peripheral monocytes.</p><p><strong>Results: </strong>Activation of monocytes from MS subjects produced significantly more IL-6 than healthy controls (49531 ± 20795 vs 10526 ± 4845), and IL-6 production trended higher in MS subjects taking DMF than those taking other DMDs (72186.9 ± 35156.2 vs 32585.8 ± 17135.4). There were no significant differences in IL-1β or TNF-α secretion.</p><p><strong>Conclusions: </strong>Our data suggest that not all DMDs may provide disease modification by suppressing monocyte/macrophage production of pro-inflammatory mediators.</p>","PeriodicalId":87318,"journal":{"name":"Journal of systems and integrative neuroscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5621757/pdf/nihms906974.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35562668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improvement of long-term memory access with a pro-dopamine regulator in an elderly male: Are we targeting dopamine tone?","authors":"Thomas McLaughlin,&nbsp;David Han,&nbsp;James Nicholson,&nbsp;Bruce Steinberg,&nbsp;Kenneth Blum,&nbsp;Marcelo Febo,&nbsp;Eric Braverman,&nbsp;Mona Li,&nbsp;Lyle Fried,&nbsp;Rajendra Badgaiyan","doi":"10.15761/JSIN.1000165","DOIUrl":"https://doi.org/10.15761/JSIN.1000165","url":null,"abstract":"<p><p>With aging, there is decline in both short-term and long-term memory. This effect is magnified by epigenetic insults on specific, dopamine- related genes (e.g., DRD2, DAT1) as well as by impaired or reduced mRNA transcription. In addition, long-term memory ability is positively correlated with dopamine function and there is evidence that aging is associated with a reduction in brain dopamine D2 receptors, with an acceleration seen in aging-induced dementia. As a result, the authors tested the acute effect of a Pro-Dopamine Regulator (KB220Z, liquid Nano variant) on an aspect of long-term memory performance in a 77-year-old, highly functional male, using the Animal Naming Test (ANT). An improvement in long-term memory retrieval had initially been noted during the subject's follow-up neurology exam, after he had been, for other reasons, taking KB220z. The patient had been given a number of ANTs by his primary and, later, another neurologist, from 2013 to 2016. Because the number of ANT observations was small (N = 7 with two groups) and the data uncorrelated, a non-parametric Wilcoxon-Mann-Whitney test was performed to test mean differences. After KB220z, the patient had much higher scores (p = 0.04762) on the ANT vs. when not taking it. His scores increased from the 30^th percentile (pre-test) to the 76^th percentile, after the first administration of KB220z and, later, to the 98^th percentile, after a second administration of KB220z, six months later. The results indicate that KB220z, given acutely, increased a form of long-term memory retrieval in a highly functional, elderly male. Larger, double-blind, randomized controlled studies are encouraged.</p>","PeriodicalId":87318,"journal":{"name":"Journal of systems and integrative neuroscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5800757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35813850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lyme and Dopaminergic Function: Hypothesizing Reduced Reward Deficiency Symptomatology by Regulating Dopamine Transmission.","authors":"Kenneth Blum,&nbsp;Edward J Modestino,&nbsp;Marcelo Febo,&nbsp;Bruce Steinberg,&nbsp;Thomas McLaughlin,&nbsp;Lyle Fried,&nbsp;David Baron,&nbsp;David Siwicki,&nbsp;Rajendra D Badgaiyan","doi":"10.15761/JSIN.1000163","DOIUrl":"https://doi.org/10.15761/JSIN.1000163","url":null,"abstract":"<p><p>The principal vector of Lyme disease in the United States is Ixodes scapularis: black legged or deer ticks. There is increased evidence that those infected may be plagued by anxiety or depression as well. Researchers have identified transcripts coding for two putative cytosolic sulfotransferases in these ticks, which recognized phenolic monoamines as their substrates. It is hypothesized that protracted Lyme disease sequelae may be due to impairment of dopaminergic function of the brain reward circuitry. The subsequent recombinant proteins exhibited sulfotransferase function against two neurotransmitters: dopamine and octopamine. This, in itself, can reduce dopamine function leading to many Reward Deficiency Syndrome behaviors, including depression and possibly, anxiety. In fact, it was shown that activity of Ixosc Sult 1 and Sult 2 in the Ixodid tick salivary glands might contain inactivation of the salivation signal through sulfonation of either dopamine or octopamine. This infraction results in a number of clinically observed mood changes, such as anxiety and depression. In fact, there are common symptoms observed for both Parkinson and Lyme diseases. The importance of understanding the mechanistic and neurobiological effects of Lyme on the central nervous system (CNS) provides the basis for pro-dopamine regulation as a treatment. WC 195.</p>","PeriodicalId":87318,"journal":{"name":"Journal of systems and integrative neuroscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5521197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35194993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}