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This document summarizes research from the National Institute on Drug Abuse (NIDA) on the effects of drugs on the brain. It contains several images from NIDA research depicting: 1) How drugs affect brain activity in different regions over time as shown through positron emission tomography scans. 2) Long term changes in brain metabolism in cocaine abusers compared to non-abusers. 3) Evidence that drug addiction has long term consequences by altering brain structure and function even after periods of abstinence.
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Nida
This document discusses how drugs affect the brain. It shows that:
1) Drugs cause large increases in dopamine levels that reinforce drug-taking behavior.
2) Continued drug use leads to long-lasting changes in the brain like decreased dopamine receptors.
3) These brain changes help explain why drug addiction is a chronic relapsing condition.
Ibogaine
Ibogaine is a psychoactive alkaloid derived from the root bark of the Tabernanthe iboga plant found in West Africa. It has been used traditionally by healers in Gabon to induce near-death experiences and has more recently been studied for its potential anti-addictive effects. Research on rats has suggested ibogaine may increase expression of GDNF, a neurotrophic factor, which could play a role in its anti-addictive mechanism of action. Clinical studies on opioid addicts found that 25-38% experienced cessation of withdrawal symptoms within 24 hours and 29% remained drug-free for 2-6 months, though more research is still needed due to safety concerns.
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a very basic introduction to Down syndrome, some therapeutic targets, and clinical trials sponsored by the Jerome Lejeune Foundation
Integrated Behavioral Health: Neuropharmacology of Addiction (Biological Basics)
This lecture explores several theories of addiction. The dopamine hypothesis, the stress hypothesis and some core findings that can lead to more effective treatment.
Contributions of Neuroscience toOur Understanding of Cogniti
Contributions of Neuroscience to
Our Understanding of Cognitive
Development
Adele Diamond1 and Dima Amso2
1
Department of Psychiatry, University of British Columbia, and Department of Child and Adolescent Psychiatry,
BC Children’s Hospital, Vancouver, Canada; and
2
Sackler Institute for Developmental Psychobiology,
Weill Medical College of Cornell University
ABSTRACT—One major contribution of neuroscience to
understanding cognitive development has been in demon-
strating that biology is not destiny—that is, demonstrating
the remarkable role of experience in shaping the mind,
brain, and body. Only rarely has neuroscience provided
wholly new insights into cognitive development, but often
it has provided evidence of mechanisms by which obser-
vations of developmental psychologists could be explained.
Behavioral findings have often remained controversial
until an underlying biological mechanism for them was
offered. Neuroscience has demonstrated promise for de-
tecting cognitive problems before they are behaviorally
observable—and, hence, promise for early intervention. In
this article, we discuss examples drawn from imitation and
mirror neurons, phenylketonuria (PKU) and prefrontal
dopamine, maternal touch and stress reactivity, and non-
genetic (behavioral) intergenerational transmission of bi-
ological characteristics.
KEYWORDS—plasticity; epigenesis; mothering; executive
functions; animal models; molecular genetics; memory
Neuroscience research has made its greatest contributions to the
study of cognitive development by illuminating mechanisms
(providing a ‘‘how’’) that underlie behavioral observations made
earlier by psychologists. It has also made important contribu-
tions to our understanding of cognitive development by dem-
onstrating that the brain is far more plastic at all ages than
previously thought—and thus that the speed and extent by which
experience and behavior can shape the brain is greater than al-
most anyone imagined. In other words, rather than showing that
biology is destiny, neuroscience research has been at the fore-
front of demonstrating the powerful role of experience throughout
life. Besides the surprising evidence of the remarkable extent
of experience-induced plasticity, rarely has neuroscience given
us previously unknown insights into cognitive development, but
neuroscience does offer promise of being able to detect some
problems before they are behaviorally observable.
PROVIDING MECHANISMS THAT CAN ACCOUNT FOR
BEHAVIORAL RESULTS REPORTED BY
PSYCHOLOGISTS
Here we describe two examples of behavioral findings by psy-
chologists that were largely ignored or extremely controversial
until underlying biological mechanisms capable of accounting
for them were provided by neuroscience research. One such
example concerns cognitive deficits documented in children
treated early and continuously for phenylketonuria (PKU). The
second example involves neonatal imitation observed b ...
Final coaching on coping with internet addiction counsellor s tool (1)
This document discusses counseling on coping with internet addiction. It begins by defining internet addiction disorder and comparing behavioral vs physiological addictions. It then discusses various researchers and scales used to study internet addiction, including the Chen Internet Addiction Scale. The document explores attempting to diagnose internet addiction using psychological tests and biomolecular tools like the protein Delta FosB. It outlines potential dangers of internet addiction seen in cases of collapsed gamers and outlines brain changes caused by addiction like dopamine downregulation.
196 CNS Neurosci Ther. 2021;27196–205.wileyonlinelibra
196 | CNS Neurosci Ther. 2021;27:196–205.wileyonlinelibrary.com/journal/cns
1 | I N T R O D U C T I O N
Addiction is a mental disorder defined by compulsive and chronic drug
taking. The development of drug abuse after an extended period of drug
taking has been suggested to depend on a shift from early recreational
drug use to later compulsive drug abuse. The neurobiological mechanisms
leading to this shift remain unknown. Furthermore, compared with a lim-
ited drug history, extended drug exposure was assumed to have a higher
probability to lead to prolonged neuronal alterations, resulting in a higher
risk of drug relapse and a further extension of drug abuse.1-4
The insular cortex (IC), or insula for short, plays an important
role in drug addiction. Both human5-7 and animal studies8 showed
Received: 30 July 2020 | Revised: 19 September 2020 | Accepted: 23 September 2020
DOI: 10.1111/cns.13469
O R I G I N A L A R T I C L E
Limited versus extended cocaine intravenous self-
administration: Behavioral effects and electrophysiological
changes in insular cortex
Yi-Xiao Luo1,2 | Donald Huang1 | Changyong Guo1 | Yao-Ying Ma1,2,3
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium,
provided the original work is properly cited.
© 2020 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd
Luo and Huang are contributed equally to this work.
1Department of Pharmacology and
Toxicology, Indiana University School of
Medicine, Indianapolis, IN, USA
2Department of Psychology, Behavioral
Neuroscience Program, State University of
New York, Binghamton, NY, USA
3Stark Neurosciences Research Institute,
Indiana University School of Medicine,
Indianapolis, IN, USA
Correspondence
Yao-Ying Ma, Department of Pharmacology
and Toxicology, Indiana University School of
Medicine, 635 Barnhill Drive, Indianapolis,
IN 46202, USA.
Email: [email protected]
Funding information
Brain & Behavior Research Foundation
grant, Grant/Award Number: 24989;
National Institute on Alcohol Abuse
and Alcoholism, Grant/Award Number:
R01AA025784
Abstract
Aims: Limited vs extended drug exposure has been proposed as one of the key factors
in determining the risk of relapse, which is the primary characteristic of addiction
behaviors. The current studies were designed to explore the related behavioral
effects and neuronal alterations in the insular cortex (IC), an important brain region
involved in addiction.
Methods: Experiments started with rats at the age of 35 days, a typical adolescent
stage when initial drug exposure occurs often in humans. The drug-seeking/taking
behaviors, and membrane properties and intrinsic excitability of IC pyramidal neurons
were measured on withdrawal day (WD) 1 and WD 45-48 after limited vs extended
cocaine intravenous self-administration (IVSA).
Results: We found higher coca ...
Recommended
Nida
This document discusses how drugs affect the brain. It shows that:
1) Drugs cause large increases in dopamine levels that reinforce drug-taking behavior.
2) Continued drug use leads to long-lasting changes in the brain like decreased dopamine receptors.
3) These brain changes help explain why drug addiction is a chronic relapsing condition.
Ibogaine
Ibogaine is a psychoactive alkaloid derived from the root bark of the Tabernanthe iboga plant found in West Africa. It has been used traditionally by healers in Gabon to induce near-death experiences and has more recently been studied for its potential anti-addictive effects. Research on rats has suggested ibogaine may increase expression of GDNF, a neurotrophic factor, which could play a role in its anti-addictive mechanism of action. Clinical studies on opioid addicts found that 25-38% experienced cessation of withdrawal symptoms within 24 hours and 29% remained drug-free for 2-6 months, though more research is still needed due to safety concerns.
A Primer on Down Syndrome Neuroscience and the Development of Therapeutic Tar...
a very basic introduction to Down syndrome, some therapeutic targets, and clinical trials sponsored by the Jerome Lejeune Foundation
Integrated Behavioral Health: Neuropharmacology of Addiction (Biological Basics)
This lecture explores several theories of addiction. The dopamine hypothesis, the stress hypothesis and some core findings that can lead to more effective treatment.
Contributions of Neuroscience toOur Understanding of Cogniti
Contributions of Neuroscience to
Our Understanding of Cognitive
Development
Adele Diamond1 and Dima Amso2
1
Department of Psychiatry, University of British Columbia, and Department of Child and Adolescent Psychiatry,
BC Children’s Hospital, Vancouver, Canada; and
2
Sackler Institute for Developmental Psychobiology,
Weill Medical College of Cornell University
ABSTRACT—One major contribution of neuroscience to
understanding cognitive development has been in demon-
strating that biology is not destiny—that is, demonstrating
the remarkable role of experience in shaping the mind,
brain, and body. Only rarely has neuroscience provided
wholly new insights into cognitive development, but often
it has provided evidence of mechanisms by which obser-
vations of developmental psychologists could be explained.
Behavioral findings have often remained controversial
until an underlying biological mechanism for them was
offered. Neuroscience has demonstrated promise for de-
tecting cognitive problems before they are behaviorally
observable—and, hence, promise for early intervention. In
this article, we discuss examples drawn from imitation and
mirror neurons, phenylketonuria (PKU) and prefrontal
dopamine, maternal touch and stress reactivity, and non-
genetic (behavioral) intergenerational transmission of bi-
ological characteristics.
KEYWORDS—plasticity; epigenesis; mothering; executive
functions; animal models; molecular genetics; memory
Neuroscience research has made its greatest contributions to the
study of cognitive development by illuminating mechanisms
(providing a ‘‘how’’) that underlie behavioral observations made
earlier by psychologists. It has also made important contribu-
tions to our understanding of cognitive development by dem-
onstrating that the brain is far more plastic at all ages than
previously thought—and thus that the speed and extent by which
experience and behavior can shape the brain is greater than al-
most anyone imagined. In other words, rather than showing that
biology is destiny, neuroscience research has been at the fore-
front of demonstrating the powerful role of experience throughout
life. Besides the surprising evidence of the remarkable extent
of experience-induced plasticity, rarely has neuroscience given
us previously unknown insights into cognitive development, but
neuroscience does offer promise of being able to detect some
problems before they are behaviorally observable.
PROVIDING MECHANISMS THAT CAN ACCOUNT FOR
BEHAVIORAL RESULTS REPORTED BY
PSYCHOLOGISTS
Here we describe two examples of behavioral findings by psy-
chologists that were largely ignored or extremely controversial
until underlying biological mechanisms capable of accounting
for them were provided by neuroscience research. One such
example concerns cognitive deficits documented in children
treated early and continuously for phenylketonuria (PKU). The
second example involves neonatal imitation observed b ...
Final coaching on coping with internet addiction counsellor s tool (1)
This document discusses counseling on coping with internet addiction. It begins by defining internet addiction disorder and comparing behavioral vs physiological addictions. It then discusses various researchers and scales used to study internet addiction, including the Chen Internet Addiction Scale. The document explores attempting to diagnose internet addiction using psychological tests and biomolecular tools like the protein Delta FosB. It outlines potential dangers of internet addiction seen in cases of collapsed gamers and outlines brain changes caused by addiction like dopamine downregulation.
196 CNS Neurosci Ther. 2021;27196–205.wileyonlinelibra
196 | CNS Neurosci Ther. 2021;27:196–205.wileyonlinelibrary.com/journal/cns
1 | I N T R O D U C T I O N
Addiction is a mental disorder defined by compulsive and chronic drug
taking. The development of drug abuse after an extended period of drug
taking has been suggested to depend on a shift from early recreational
drug use to later compulsive drug abuse. The neurobiological mechanisms
leading to this shift remain unknown. Furthermore, compared with a lim-
ited drug history, extended drug exposure was assumed to have a higher
probability to lead to prolonged neuronal alterations, resulting in a higher
risk of drug relapse and a further extension of drug abuse.1-4
The insular cortex (IC), or insula for short, plays an important
role in drug addiction. Both human5-7 and animal studies8 showed
Received: 30 July 2020 | Revised: 19 September 2020 | Accepted: 23 September 2020
DOI: 10.1111/cns.13469
O R I G I N A L A R T I C L E
Limited versus extended cocaine intravenous self-
administration: Behavioral effects and electrophysiological
changes in insular cortex
Yi-Xiao Luo1,2 | Donald Huang1 | Changyong Guo1 | Yao-Ying Ma1,2,3
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium,
provided the original work is properly cited.
© 2020 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd
Luo and Huang are contributed equally to this work.
1Department of Pharmacology and
Toxicology, Indiana University School of
Medicine, Indianapolis, IN, USA
2Department of Psychology, Behavioral
Neuroscience Program, State University of
New York, Binghamton, NY, USA
3Stark Neurosciences Research Institute,
Indiana University School of Medicine,
Indianapolis, IN, USA
Correspondence
Yao-Ying Ma, Department of Pharmacology
and Toxicology, Indiana University School of
Medicine, 635 Barnhill Drive, Indianapolis,
IN 46202, USA.
Email: [email protected]
Funding information
Brain & Behavior Research Foundation
grant, Grant/Award Number: 24989;
National Institute on Alcohol Abuse
and Alcoholism, Grant/Award Number:
R01AA025784
Abstract
Aims: Limited vs extended drug exposure has been proposed as one of the key factors
in determining the risk of relapse, which is the primary characteristic of addiction
behaviors. The current studies were designed to explore the related behavioral
effects and neuronal alterations in the insular cortex (IC), an important brain region
involved in addiction.
Methods: Experiments started with rats at the age of 35 days, a typical adolescent
stage when initial drug exposure occurs often in humans. The drug-seeking/taking
behaviors, and membrane properties and intrinsic excitability of IC pyramidal neurons
were measured on withdrawal day (WD) 1 and WD 45-48 after limited vs extended
cocaine intravenous self-administration (IVSA).
Results: We found higher coca ...
Voth presentation
Marijuana use among youth poses significant risks to brain development and mental health. Regular marijuana use is associated with cognitive decline across all domains even after years of abstinence. It can also increase the likelihood of developing psychiatric disorders like depression and psychosis. Prenatal marijuana exposure has been linked to lower birth weight, abnormal development and long term cognitive impairments in offspring. Overall, the evidence shows that marijuana jeopardizes the healthy development of youth.
330 www.thelancet.comneurology Vol 13 March 2014Revie.docx
330 www.thelancet.com/neurology Vol 13 March 2014
Review
Neurobehavioural eff ects of developmental toxicity
Philippe Grandjean, Philip J Landrigan
Neurodevelopmental disabilities, including autism, attention-defi cit hyperactivity disorder, dyslexia, and other
cognitive impairments, aff ect millions of children worldwide, and some diagnoses seem to be increasing in frequency.
Industrial chemicals that injure the developing brain are among the known causes for this rise in prevalence. In 2006,
we did a systematic review and identifi ed fi ve industrial chemicals as developmental neurotoxicants: lead,
methylmercury, polychlorinated biphenyls, arsenic, and toluene. Since 2006, epidemiological studies have documented
six additional developmental neurotoxicants—manganese, fl uoride, chlorpyrifos, dichlorodiphenyltrichloroethane,
tetrachloroethylene, and the polybrominated diphenyl ethers. We postulate that even more neurotoxicants remain
undiscovered. To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy.
Untested chemicals should not be presumed to be safe to brain development, and chemicals in existing use and all
new chemicals must therefore be tested for developmental neurotoxicity. To coordinate these eff orts and to accelerate
translation of science into prevention, we propose the urgent formation of a new international clearinghouse.
Introduction
Disorders of neurobehavioural development aff ect 10–15%
of all births,1 and prevalence rates of autism spectrum
disorder and attention-defi cit hyperactivity disorder seem
to be increasing worldwide.2 Subclinical decrements in
brain function are even more common than these
neurobehavioural developmental disorders. All these
disabilities can have severe consequences3—they diminish
quality of life, reduce academic achievement, and disturb
behaviour, with profound consequences for the welfare
and productivity of entire societies.4
The root causes of the present global pandemic of
neurodevelopmental disorders are only partly
understood. Although genetic factors have a role,5 they
cannot explain recent increases in reported prevalence,
and none of the genes discovered so far seem to be
responsible for more than a small proportion of cases.5
Overall, genetic factors seem to account for no more than
perhaps 30–40% of all cases of neurodevelopmental
disorders. Thus, non-genetic, environmental exposures
are involved in causation, in some cases probably by
interacting with genetically inherited predispositions.
Strong evidence exists that industrial chemicals widely
disseminated in the environment are important
contributors to what we have called the global, silent
pandemic of neurodevelopmental toxicity.6,7 The
developing human brain is uniquely vulnerable to toxic
chemical exposures, and major windows of
developmental vulnerability occur in utero and during
infancy and early childhood.8 During these sensitive life ...
Comment on microglia
Comment on the publication Microglial Activity in People at Ultra High Risk of Psychosis and in Schizophrenia: An [11C]PBR28 PET Brain Imaging Study, with reference to the publication NEUROIMMUNE MECHANISMS IN FETAL ALCOHOL SPECTRUM DISORDER
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This document summarizes research on drug abuse and addiction. It finds that addiction is a brain disease characterized by compulsive drug use despite negative consequences. Addiction involves changes in brain structure and function that compromise mental and motor function if untreated. Multiple factors contribute to addiction risk including genetics, environment, development, mental illness and stress. Effective prevention and treatment strategies must address the biological, psychological and social aspects of addiction over the long term, as addiction is a chronic and relapsing disease. International research collaboration is needed to address drug abuse globally.
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This document summarizes research on drug abuse and addiction. It finds that addiction is a brain disease characterized by compulsive drug use despite negative consequences. Addiction involves changes in brain structure and function that persist even after periods of abstinence. Risk factors include genetics, mental illness, stress, and drug availability. Prevention and treatment strategies must consider biological, psychological, and social factors. Addiction is treatable, but often requires multiple treatment attempts due to high relapse rates, similar to other chronic diseases. Further research aims to develop improved prevention and treatment methods.
SNONewsVol3Issue1
The 16th Annual Scientific Meeting of the Society for Neuro-Oncology and AANS/CNS Section on Tumors was held November 17-20, 2011 in Orange County, CA. Over 1300 participants from 37 countries attended the four day meeting focused on the latest laboratory and clinical research in neuro-oncology. The meeting included education day sessions, morning and afternoon oral presentation sessions on various topics, keynote addresses, award presentations, and poster sessions to facilitate the multidisciplinary exchange of ideas. The successful annual meeting brought together neuro-oncologists, surgeons, pathologists, and other specialists to advance the research, diagnosis, care and treatment of brain tumors.
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This document provides an overview of addiction and the neuroscience of addiction. It begins by defining addiction as a chronically relapsing disorder characterized by compulsion to seek a stimulus, loss of control, and negative emotional state during withdrawal. It discusses compulsive drug use and the neurobiology of the binge/intoxication, withdrawal/negative affect, and preoccupation/craving stages of addiction. It provides data on the prevalence and societal costs of various addictions. It also summarizes current and potential medications to treat the positive and negative reinforcing aspects of addiction.
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This document summarizes research on the maturation of the adolescent brain. It finds that the brain remains in an active state of development during adolescence, particularly in the limbic system which impacts risk-taking behaviors. Magnetic resonance imaging studies show that myelination and development of neurocircuitry, which are influenced by sex hormones, continue into adolescence. As a result, the adolescent brain exhibits impulsive behaviors and is vulnerable to substance abuse due to an immature prefrontal cortex and limbic system. Factors like genetics, environment, nutrition, sleep, and stress can also influence adolescent brain maturation.
Analyzing the neuroprotective potential of nicotine in Parkinson's Disease (P...
Nicotine may serve as a neuroprotective agent for Parkinson's disease (PD) by protecting dopamine neurons from further degeneration. This literature review analyzed 10 peer-reviewed animal studies that investigated the effects of nicotine administration on dopamine levels and motor symptoms in rodent and primate models of PD. The majority of studies found that nicotine did not increase dopamine levels directly but served as a neuroprotective factor by preventing further dopamine neuron loss. Three studies reported that nicotine did increase striatal dopamine levels. Most studies also found that intermittent nicotine treatment was more effective than chronic treatment at reducing motor symptoms. However, more research is needed to determine if nicotine can also help treat non-motor PD symptoms.
Poster
Fetal nigral transplantation involves surgically transplanting dopamine-producing neurons from human fetal tissue grafts into the brains of Parkinson's disease patients. This aims to reinnervate the dopamine-depleted striatum and restore motor function. Studies have found the grafts can survive long-term, improve motor symptoms, and allow some patients to reduce their need for dopamine medication. However, fetal tissue transplantation still carries risks of dyskinesia and varying degrees of success, and is unlikely to become a routine therapy for Parkinson's disease.
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Researchers at Brown University conducted a study using fruit flies to investigate alcohol addiction on a molecular level. They found that alcohol hijacks a conserved memory pathway in the brain responsible for euphoric recall, altering genes in this pathway and forming cravings. This explains why alcoholics continue to experience cravings even after abstaining, as their brain only recalls the rewarding effects of alcohol rather than the negative effects. The study concludes that alcoholism is caused by chemical changes to the brain's reward system from repeated alcohol exposure, leaving alcoholics powerless over their addiction. Further research is still needed to fully understand the factors influencing individual predispositions to developing alcoholism.
Journal.pbio.2006497
Universidad Estatal de Florida en Tallahassee, demostró que el consumo de nicotina de los padres puede causar problemas cognitivos en sus hijos y sus nietos.
Presentation Finalwithnotes
The document discusses sleepwalking and summarizes several key points:
1) Sleepwalking occurs when there are "hypersynchronous bursts of delta activity" in the brain compared to normal sleep, along with increased blood flow to certain brain regions and decreased flow to others.
2) Several social factors can influence sleepwalking, including stress, lack of sleep, substance abuse, hormone changes, and illness.
3) Both stress and sleep loss can negatively impact physical and mental health, especially in children, by impairing cognitive function and increasing illness risk.
4) Genetic factors are involved in sleepwalking, which is more likely to be manifested in children whose parents also experienced sleepwalking as children.
Xyzmusts to know about internet addiction (1)
This document discusses internet addiction and provides an overview of the topic. It begins by outlining how internet addiction came to be studied as a disorder and some of the key players in the field. It then discusses attempts to diagnose internet addiction using psychological tests and molecular tools like examining Delta FosB expression. The dangers of internet addiction are examined by looking at case studies and the biological mechanisms involved like dopamine dysregulation. The document ends by proposing future directions for research, including examining the epigenetic factors related to increased vulnerability to internet addiction.
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This document discusses the biological aspects and theories of schizophrenia. It covers genetic factors, brain structure abnormalities, and biochemical factors like the dopamine hypothesis. Twin and adoption studies provide evidence for genetic influences. Post-mortem and imaging studies show reductions in brain areas like the hippocampus, amygdala and prefrontal cortex. The dopamine hypothesis proposes elevated dopamine levels in schizophrenia patients. Other neurotransmitters like serotonin, norepinephrine and glutamate may also play a role. No single cause has been identified and it is likely that both genetic and environmental factors contribute to the development of schizophrenia.
Icci Evolutive immunologic and toxicologic approach in some neuroinflammatory...
Icci Evolutive immunologic and toxicologic approach in some neuroinflammatory...M. Luisetto Pharm.D.Spec. Pharmacology
This document discusses the evolutionary perspective on neurodegenerative diseases like Parkinson's disease (PD). It proposes that PD is uniquely human because of the massive expansion of dopamine neurons in the human brain compared to other mammals. This neuronal overload may explain the selective fragility seen in PD. While no spontaneous movement disorders are seen in other mammals, useful animal models of PD exist. Reasons for the increasing prevalence of PD in humans over history include longer lifespans and reduced physical activity levels impacting neurotrophic factors. Brain evolution in vertebrates led to increased complexity and new structures, which may have created vulnerabilities underlying certain neurodegenerative diseases.Effective usage of Led bulbs and Artificial Lights: Its Pathophysiological co...
Effective usage of Led bulbs and Artificial Lights: Its Pathophysiological co...Chiranjeevi JIPMER Puducherry
Objective and Study Design: This was a cross-sectional study purposed to observe the effects of led bulbs and artificial lights on human health and its physiological considerations on sleep.
Our study addressed two goals. Our first goal was to determine the extent to which light pollution was perceived as a problem by the people. Our second goal was to recommend
applicable lighting ordinances for reducing light pollution. Material and Methods: This study was conducted at All India Institute of Medical Sciences hospital, Bhopal and Narayana medical college, Nellore during the period between May 2014 and August 2015. Three hundred human volunteers, 123 female and 177 male, ages of 18 and 55 were studied in a two-part experiment, which included one Sleep questionnaire regarding light pollution to study each individual's
normal body conditions, and an Assay of melatonin in saliva. Results: The results showed that many participants have a long history of sleeping problems. They usually take at least an hour to fall asleep and tend to wake up frequently throughout the night and feel poorly rested in the morning. The salivary melatonin levels also declined at night due to progressive exposure to artificial light. Conclusion: Through our research, we have obtained data that strongly suggest that light pollution is adversely affecting public health, causing them to experience sleep loss, visual fatigue, weariness, anxiety, and depression.Essay 5- Mental
1) Schizophrenia is a mental disorder characterized by auditory hallucinations, delusional thoughts, and emotional changes. A major identifiable cause is a heritable genetic component.
2) Research has found links between specific genes and schizophrenia, as well as higher likelihood of developing the disorder in closer relatives.
3) Studying endophenotypes, or heritable biomarkers related to but not specific to the illness, may help identify genetic causes and allow research on a smaller scale prior to full diagnosis. This could help advance understanding and potential prevention of schizophrenia.
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Neurological system includes brain and spinal cord. It plays an important role in functioning of our body. Encephalitis is the inflammation of the brain. Causes include viral infections, infections from insect bites or an autoimmune reaction that affects the brain. It can be life-threatening or cause long-term complications. Treatment varies, but most people require hospitalization so they can receive intensive treatment, including life support.
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Voth presentation
Marijuana use among youth poses significant risks to brain development and mental health. Regular marijuana use is associated with cognitive decline across all domains even after years of abstinence. It can also increase the likelihood of developing psychiatric disorders like depression and psychosis. Prenatal marijuana exposure has been linked to lower birth weight, abnormal development and long term cognitive impairments in offspring. Overall, the evidence shows that marijuana jeopardizes the healthy development of youth.
330 www.thelancet.comneurology Vol 13 March 2014Revie.docx
330 www.thelancet.com/neurology Vol 13 March 2014
Review
Neurobehavioural eff ects of developmental toxicity
Philippe Grandjean, Philip J Landrigan
Neurodevelopmental disabilities, including autism, attention-defi cit hyperactivity disorder, dyslexia, and other
cognitive impairments, aff ect millions of children worldwide, and some diagnoses seem to be increasing in frequency.
Industrial chemicals that injure the developing brain are among the known causes for this rise in prevalence. In 2006,
we did a systematic review and identifi ed fi ve industrial chemicals as developmental neurotoxicants: lead,
methylmercury, polychlorinated biphenyls, arsenic, and toluene. Since 2006, epidemiological studies have documented
six additional developmental neurotoxicants—manganese, fl uoride, chlorpyrifos, dichlorodiphenyltrichloroethane,
tetrachloroethylene, and the polybrominated diphenyl ethers. We postulate that even more neurotoxicants remain
undiscovered. To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy.
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new chemicals must therefore be tested for developmental neurotoxicity. To coordinate these eff orts and to accelerate
translation of science into prevention, we propose the urgent formation of a new international clearinghouse.
Introduction
Disorders of neurobehavioural development aff ect 10–15%
of all births,1 and prevalence rates of autism spectrum
disorder and attention-defi cit hyperactivity disorder seem
to be increasing worldwide.2 Subclinical decrements in
brain function are even more common than these
neurobehavioural developmental disorders. All these
disabilities can have severe consequences3—they diminish
quality of life, reduce academic achievement, and disturb
behaviour, with profound consequences for the welfare
and productivity of entire societies.4
The root causes of the present global pandemic of
neurodevelopmental disorders are only partly
understood. Although genetic factors have a role,5 they
cannot explain recent increases in reported prevalence,
and none of the genes discovered so far seem to be
responsible for more than a small proportion of cases.5
Overall, genetic factors seem to account for no more than
perhaps 30–40% of all cases of neurodevelopmental
disorders. Thus, non-genetic, environmental exposures
are involved in causation, in some cases probably by
interacting with genetically inherited predispositions.
Strong evidence exists that industrial chemicals widely
disseminated in the environment are important
contributors to what we have called the global, silent
pandemic of neurodevelopmental toxicity.6,7 The
developing human brain is uniquely vulnerable to toxic
chemical exposures, and major windows of
developmental vulnerability occur in utero and during
infancy and early childhood.8 During these sensitive life ...
Comment on microglia
Comment on the publication Microglial Activity in People at Ultra High Risk of Psychosis and in Schizophrenia: An [11C]PBR28 PET Brain Imaging Study, with reference to the publication NEUROIMMUNE MECHANISMS IN FETAL ALCOHOL SPECTRUM DISORDER
addiction science.ppt
This document summarizes research on drug abuse and addiction. It finds that addiction is a brain disease characterized by compulsive drug use despite negative consequences. Addiction involves changes in brain structure and function that compromise mental and motor function if untreated. Multiple factors contribute to addiction risk including genetics, environment, development, mental illness and stress. Effective prevention and treatment strategies must address the biological, psychological and social aspects of addiction over the long term, as addiction is a chronic and relapsing disease. International research collaboration is needed to address drug abuse globally.
Neurobiology of drug abuse and addiction_NIDA
This document summarizes research on drug abuse and addiction. It finds that addiction is a brain disease characterized by compulsive drug use despite negative consequences. Addiction involves changes in brain structure and function that persist even after periods of abstinence. Risk factors include genetics, mental illness, stress, and drug availability. Prevention and treatment strategies must consider biological, psychological, and social factors. Addiction is treatable, but often requires multiple treatment attempts due to high relapse rates, similar to other chronic diseases. Further research aims to develop improved prevention and treatment methods.
SNONewsVol3Issue1
The 16th Annual Scientific Meeting of the Society for Neuro-Oncology and AANS/CNS Section on Tumors was held November 17-20, 2011 in Orange County, CA. Over 1300 participants from 37 countries attended the four day meeting focused on the latest laboratory and clinical research in neuro-oncology. The meeting included education day sessions, morning and afternoon oral presentation sessions on various topics, keynote addresses, award presentations, and poster sessions to facilitate the multidisciplinary exchange of ideas. The successful annual meeting brought together neuro-oncologists, surgeons, pathologists, and other specialists to advance the research, diagnosis, care and treatment of brain tumors.
Dr. koob connect presentation
This document provides an overview of addiction and the neuroscience of addiction. It begins by defining addiction as a chronically relapsing disorder characterized by compulsion to seek a stimulus, loss of control, and negative emotional state during withdrawal. It discusses compulsive drug use and the neurobiology of the binge/intoxication, withdrawal/negative affect, and preoccupation/craving stages of addiction. It provides data on the prevalence and societal costs of various addictions. It also summarizes current and potential medications to treat the positive and negative reinforcing aspects of addiction.
Cerebro adolescente
This document summarizes research on the maturation of the adolescent brain. It finds that the brain remains in an active state of development during adolescence, particularly in the limbic system which impacts risk-taking behaviors. Magnetic resonance imaging studies show that myelination and development of neurocircuitry, which are influenced by sex hormones, continue into adolescence. As a result, the adolescent brain exhibits impulsive behaviors and is vulnerable to substance abuse due to an immature prefrontal cortex and limbic system. Factors like genetics, environment, nutrition, sleep, and stress can also influence adolescent brain maturation.
Analyzing the neuroprotective potential of nicotine in Parkinson's Disease (P...
Nicotine may serve as a neuroprotective agent for Parkinson's disease (PD) by protecting dopamine neurons from further degeneration. This literature review analyzed 10 peer-reviewed animal studies that investigated the effects of nicotine administration on dopamine levels and motor symptoms in rodent and primate models of PD. The majority of studies found that nicotine did not increase dopamine levels directly but served as a neuroprotective factor by preventing further dopamine neuron loss. Three studies reported that nicotine did increase striatal dopamine levels. Most studies also found that intermittent nicotine treatment was more effective than chronic treatment at reducing motor symptoms. However, more research is needed to determine if nicotine can also help treat non-motor PD symptoms.
Poster
Fetal nigral transplantation involves surgically transplanting dopamine-producing neurons from human fetal tissue grafts into the brains of Parkinson's disease patients. This aims to reinnervate the dopamine-depleted striatum and restore motor function. Studies have found the grafts can survive long-term, improve motor symptoms, and allow some patients to reduce their need for dopamine medication. However, fetal tissue transplantation still carries risks of dyskinesia and varying degrees of success, and is unlikely to become a routine therapy for Parkinson's disease.
Alcohol Hijacks The Brain Study Finds
Researchers at Brown University conducted a study using fruit flies to investigate alcohol addiction on a molecular level. They found that alcohol hijacks a conserved memory pathway in the brain responsible for euphoric recall, altering genes in this pathway and forming cravings. This explains why alcoholics continue to experience cravings even after abstaining, as their brain only recalls the rewarding effects of alcohol rather than the negative effects. The study concludes that alcoholism is caused by chemical changes to the brain's reward system from repeated alcohol exposure, leaving alcoholics powerless over their addiction. Further research is still needed to fully understand the factors influencing individual predispositions to developing alcoholism.
Journal.pbio.2006497
Universidad Estatal de Florida en Tallahassee, demostró que el consumo de nicotina de los padres puede causar problemas cognitivos en sus hijos y sus nietos.
Presentation Finalwithnotes
The document discusses sleepwalking and summarizes several key points:
1) Sleepwalking occurs when there are "hypersynchronous bursts of delta activity" in the brain compared to normal sleep, along with increased blood flow to certain brain regions and decreased flow to others.
2) Several social factors can influence sleepwalking, including stress, lack of sleep, substance abuse, hormone changes, and illness.
3) Both stress and sleep loss can negatively impact physical and mental health, especially in children, by impairing cognitive function and increasing illness risk.
4) Genetic factors are involved in sleepwalking, which is more likely to be manifested in children whose parents also experienced sleepwalking as children.
Xyzmusts to know about internet addiction (1)
This document discusses internet addiction and provides an overview of the topic. It begins by outlining how internet addiction came to be studied as a disorder and some of the key players in the field. It then discusses attempts to diagnose internet addiction using psychological tests and molecular tools like examining Delta FosB expression. The dangers of internet addiction are examined by looking at case studies and the biological mechanisms involved like dopamine dysregulation. The document ends by proposing future directions for research, including examining the epigenetic factors related to increased vulnerability to internet addiction.
Holding Hands With The Hopeless Edps Project Final
This was initially completed as a project in one of my courses. However, understanding substance abuse as a disease and not a moral issue or lack of willpower is vitaly important to continue to make advancements in treatments and reimbursement issues, which are a huge threat.
Hippocampal neurogenesis in_the_c57_bl_6j
Another paper that shows the effects of prenatal alcohol exposure on the development and function of the Hippocampus, with consequent memory deficiencies.
Biological aspects of schizophrenia
This document discusses the biological aspects and theories of schizophrenia. It covers genetic factors, brain structure abnormalities, and biochemical factors like the dopamine hypothesis. Twin and adoption studies provide evidence for genetic influences. Post-mortem and imaging studies show reductions in brain areas like the hippocampus, amygdala and prefrontal cortex. The dopamine hypothesis proposes elevated dopamine levels in schizophrenia patients. Other neurotransmitters like serotonin, norepinephrine and glutamate may also play a role. No single cause has been identified and it is likely that both genetic and environmental factors contribute to the development of schizophrenia.
Icci Evolutive immunologic and toxicologic approach in some neuroinflammatory...
Icci Evolutive immunologic and toxicologic approach in some neuroinflammatory...M. Luisetto Pharm.D.Spec. Pharmacology
This document discusses the evolutionary perspective on neurodegenerative diseases like Parkinson's disease (PD). It proposes that PD is uniquely human because of the massive expansion of dopamine neurons in the human brain compared to other mammals. This neuronal overload may explain the selective fragility seen in PD. While no spontaneous movement disorders are seen in other mammals, useful animal models of PD exist. Reasons for the increasing prevalence of PD in humans over history include longer lifespans and reduced physical activity levels impacting neurotrophic factors. Brain evolution in vertebrates led to increased complexity and new structures, which may have created vulnerabilities underlying certain neurodegenerative diseases.Effective usage of Led bulbs and Artificial Lights: Its Pathophysiological co...
Effective usage of Led bulbs and Artificial Lights: Its Pathophysiological co...Chiranjeevi JIPMER Puducherry
Objective and Study Design: This was a cross-sectional study purposed to observe the effects of led bulbs and artificial lights on human health and its physiological considerations on sleep.
Our study addressed two goals. Our first goal was to determine the extent to which light pollution was perceived as a problem by the people. Our second goal was to recommend
applicable lighting ordinances for reducing light pollution. Material and Methods: This study was conducted at All India Institute of Medical Sciences hospital, Bhopal and Narayana medical college, Nellore during the period between May 2014 and August 2015. Three hundred human volunteers, 123 female and 177 male, ages of 18 and 55 were studied in a two-part experiment, which included one Sleep questionnaire regarding light pollution to study each individual's
normal body conditions, and an Assay of melatonin in saliva. Results: The results showed that many participants have a long history of sleeping problems. They usually take at least an hour to fall asleep and tend to wake up frequently throughout the night and feel poorly rested in the morning. The salivary melatonin levels also declined at night due to progressive exposure to artificial light. Conclusion: Through our research, we have obtained data that strongly suggest that light pollution is adversely affecting public health, causing them to experience sleep loss, visual fatigue, weariness, anxiety, and depression.Essay 5- Mental
1) Schizophrenia is a mental disorder characterized by auditory hallucinations, delusional thoughts, and emotional changes. A major identifiable cause is a heritable genetic component.
2) Research has found links between specific genes and schizophrenia, as well as higher likelihood of developing the disorder in closer relatives.
3) Studying endophenotypes, or heritable biomarkers related to but not specific to the illness, may help identify genetic causes and allow research on a smaller scale prior to full diagnosis. This could help advance understanding and potential prevention of schizophrenia.
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powerofscience.ppt
- 1. NIDA’s mission is to bring the power of science to bear on drug abuse and addiction. Photo courtesy of NIDA.
- 2. Photo courtesy of the NIDA Web site. From A Slide Teaching Packet: The Brain and the Actions of Cocaine, Opiates, and Marijuana.
- 3. Illustration used with permission, courtesy of Lydia V. Kibiuk and the Society for Neuroscience.
- 4. Photo courtesy of the NIDA Web site. From A Slide Teaching Packet: The Brain and the Actions of Cocaine, Opiates, and Marijuana.
- 5. Photo courtesy of the NIDA Web site. From A Slide Teaching Packet: The Brain and the Actions of Cocaine, Opiates, and Marijuana.
- 6. Positron Emission Tomography (PET)
- 7. Your Brain on Drugs 1-2 Min 3-4 5-6 6-7 7-8 8-9 9-10 10-20 20-30 Photo courtesy of Nora Volkow, Ph.D. Mapping cocaine binding sites in human and baboon brain in vivo. Fowler JS, Volkow ND, Wolf AP, Dewey SL, Schlyer DJ, Macgregor RIR, Hitzemann R, Logan J, Bendreim B, Gatley ST. et al. Synapse 1989;4(4):371-377.
- 8. Your Brain After Drugs Normal Cocaine Abuser (10 days) Cocaine Abuser (100 days) Photo courtesy of Nora Volkow, Ph.D. Volkow ND, Hitzemann R, Wang C-I, Fowler IS, Wolf AP, Dewey SL. Long-term frontal brain metabolic changes in cocaine abusers. Synapse 11:184-190, 1992; Volkow ND, Fowler JS, Wang G-J, Hitzemann R, Logan J, Schlyer D, Dewey 5, Wolf AP. Decreased dopamine D2 receptor availability is associated with reduced frontal metabolism in cocaine abusers. Synapse 14:169-177, 1993.
- 9. Drugs Have Long-term Consequences Photo courtesy of NIDA from research conducted by Melega WP, Raleigh MJ, Stout DB, Lacan C, Huang SC, Phelps ME.
- 10. The Memory of Drugs Nature Video Cocaine Video Front of Brain Back of Brain Amygdala not lit up Amygdala activated Photo courtesy of Anna Rose Childress, Ph.D.
- 11. The good news is… Drug Abuse is a preventable behavior and Drug Addiction is a treatable disease Courtesy of Partnership for a Drug Free America.
- 12. … Is it worth the risk? Photo courtesy of NIDA.
- 13. Visit NIDA’s Web Site at: http://www.drugabuse.gov Photo courtesy of NIDA
- 14. Have you changed your mind? Photo courtesy of NIDA. If You Change Your Mind. Student magazine. NIH Publication No. 93-3474, 1993.