Chapter 14 - Quiz 5 Flashcards

1
Q

14.1: Substance abuse: Drug mechanisms

What is an antagonist drug?

A

-a drug that blocks a NT when it binds to a receptor (inhibit)

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2
Q

14.1: Substance abuse: Drug mechanisms

What is an agonist drug?

A

-a substance that binds to a receptor and activates it causing the drug to either mimic or increase the effects of a NT (activate)

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3
Q

14.1: Substance abuse: Drug mechanisms

When would you say a drug has an affinity for a receptor? What strength do affinities vary between? (2)

A

-a drug has an affinity for a receptor if it binds to it, like a key into a lock
-affinities vary from strong to weak

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4
Q

14.1: Substance abuse: Drug mechanisms

What is a drug’s efficacy? A drug that binds to a receptor but fails to stimulate it would have a what? (2)

A

-efficacy is the drugs tendency to activate the receptor
-it would have a high affinity but low efficacy

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5
Q

14.1: Substance abuse: Drug mechanisms

Why does a drug effect one person more than another?

A

-we have different amounts of receptors, one person may have more D4 receptors than another

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6
Q

14.1 Substance abuse: Genetic Influences

Discuss the gene that has a well-confirmed influence on alcohol abuse. What does it control? Describe this pathway. What happens in people with this gene to this pathway? What are the symptoms of this? (4)

A

-it controls the metabolism of alcohol
-after anyone drinks ethyl alcohol, enzyme in the liver turn it into acetaldehyde (toxic) and then an enzyme (acetaldehyde dehydrogenase) turns it into acetic acid (energy chemical)
-people with this gene metabolize acetaldehyde very slowly
-symptoms include flushing of the face, increased heart rate, nausea, headache, abdominal pain, impaired breathing and tissue damage

-nicknamed Asian flush

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7
Q

14.1 Substance Abuse: Environmental influences

Discuss what studies have shown about the prenatal environment and substance abuse.

A

-a mother who drinks alcohol during pregnancy increases the probability that her child will develop alcoholism later, independetly from the effect of how much she drinks as the child is growing up

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8
Q

14.1 Substance Abuse: Environmental influences

Describe the general rule for early-onset alcoholism and people with a later-onset. (2)

A

-As a rule, people with early-onset alcoholism (before age 25) have a family history of alcoholism, a genetic predisposition, and a rapid onset of the problem.
-People with later onset are more likely to have reacted to life difficulties, less likely to have a family history of alcoholism, and more likely to respond well to treatment

-Childhood environment is critical also. Children who grow up in families with careful parental supervision are much less likely to develop impulse problems, even if they have genes linked to alcohol abuse or antisocial behavior

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9
Q

14.1 Substance Abuse: Behavioral Predictors of Abuse

How do sons of alcoholics differ behaviorally, on average, from sons of nonalcoholics? How does this relate with substance abuse later in life? (2)

A

-Sons of alcoholics show less intoxication, including less body sway, after drinking a moderate amount of alcohol.
-Follow-up studies have found that men who report low intoxication after moderate drinking are more likely than others to abuse alcohol throughout their lives

-other studies looking at behavioral predictors identify these in childhood: Such studies find that alcoholism is more likely among those who were described in childhood as impulsive, risk taking, easily bored, sensation seeking, and outgoing

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10
Q

14.1 Synaptic Mechanisms: The Role of Dopamine

What did Olds and Milner discover and how does this relate to self-stimulation of the brain? (2)

A

-they discovered an area in rats brains (nucleus accumbens) that relates to reward and the release of dopamine
-they gave rats the options to self-stimulate their brain and rats did this a lot

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11
Q

14.1 Synaptic Mechanisms: The Role of Dopamine

List some of the things that prolong or increase the release of dopamine in the nucleus accumbens. (7)

A

-stimulant drugs such as cocaine and amphetamine
-sex
-music
-sugar
-imagining something pleasant
-gambling activates this area for habitual gamblers
-same for habitual video gamers

-these reults suggest that dopamine release might be essential for all addictions and substance abuse

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12
Q

14.1 Synaptic Mechanisms: The Role of Dopamine

What evidence shows that researchers hae been overemphasizing the role of dopamine? (2)

A

-although alcohol, marijuana, nicotine and opiates do generally increase dopamine release, they do not icnrease it by much and the amount of dopamine release does not correlate strongly with the pleasantness of the experience of the probability of addiction
-pharmaceutical companies have failed to find drugs that would alleviate addictions via effects on dopamine and drugs that block dopamine synapses do not reduce the reward properties of opiate drugs and they do not decrease use

-although dopamine certainly contributes to reinforcement it no longer appears to be as central as previously believed

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13
Q

14.1 Synaptic Mechanisms: Cravings

During a period of abstinence from cocaine, what happens in the nucleus accumbens? What is the result? (2)

A

-Certain glutamate synapses in the nucleus accumbens become more responsive, causing increased excitation in response to cues associated with the substance.
-The result is craving, which increases for some time during abstinence and then decreases

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14
Q

14.1 Synaptic Mechanisms: Tolerance and Withdrawal

Define tolerance

A

-as an addiction develops, many of its effects, especially the enjoyable effects, decrease. This is tolerance.

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15
Q

14.1 Synaptic Mechanisms: Tolerance and Withdrawal

What is withdrawal?

A

-when the body reacts strongly when a drug is absent because it has come to expect the drug under certain circumstances

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16
Q

14.1 Synaptic Mechanisms: Tolerance and Withdrawal

Someone who is quitting an addictive substance for the first time is strongly counseled not to try it again. Why?

A

-Taking an addictive drug during the withdrawal period is likely to lead to a habit of using the drug to relieve other kinds of distress as the drug relieves the stress of withdrawal

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17
Q

14.1 Treatments: Medications to Combat Alcohol Abuse

What is the drug disulfiram (Antabuse) and what does it do? (2)

A

-it antagonizes the enzyme that metabolizes acetaldehyde
-anyone who takes it becomes nauseated after drinking alcohol

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18
Q

14.1 Treatments: Medications to Combat Alcohol Abuse

What have most studies found about Antabuse? Does it work well for quitting alcohol abuse? (2)

A

-it is about equal to a placebo, because when people think the placebo might be Antabuse it makes the placebo effective
-Someone who takes an Antabuse pill and then drinks alcohol anyway becomes ill, and in most cases quits taking Antabuse instead of quitting alcohol.

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19
Q

14.1 Treatments: Medications to Combat Alcohol Abuse

What are the treatments listed in the textbook for combatting alcohol abuse?

A

-Antabuse
-A drug that produces nauseau after drinking
-naloxone and naltrexone

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20
Q

14.1 Treatments: Medications to combat opiate abuse

What are the two medications used to combat opiate addiction? (2)

A

-methadone
-Buprenorphine and Levomethadyl acetate (LAAM)

-however these drugs do not end the addiciton. They merely satisfy the craving in a less dangerous way

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21
Q

14.1 Treatments: Medications to combat opiate abuse

What are the benefits of methadone? (3)

A

-it activates the same brain receptors as heroin and morphine and produces the same effects
-can only be taken orally (no needles)
-it gradually enters the blood and is metabolized slowly so the withdrawal symptoms are gradual

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22
Q

14.2 Major Depressive Disorder:

What do people with MDD feel? What happens to their nucleus accumbens? What cognitive problems do they show? (3)

A

-sad and helpless most of the day every day for weeks at a time, wrothless, contemplate suicide and have trouble sleeping
-their nucleus accumbens becomes less responsive to reward
-low motivation, attention problems, impaired memory and impaired sense of smell

-studies have found people with depression more have an absence of happiness rather than increased sadness, they report less happy moments

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23
Q

14.2 Major Depressive Disorder: Genetics

What evidence suggests two types of depression are influenced by different genes?

A

-Relatives of people with early-onset depression have a high risk of depression and many other psychological disorders. Relatives of people with late-onset depression have a high probability of circulatory problems.

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24
Q

14.2 Major Depressive Disorder: Genetics

What did Caspi and colleagues report to be the relationship between depression and genetics?

A

-People with the short form of the gene controlling the serotonin transporter are more likely than other people to react to stressful experiences by becoming depressed. However, in the absence of stressful experiences, their probability is not increased.

-this gene also caused people to be more emotionally reactive to any event including happy ones or angry ones

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25
Q

14.2 Major Depressive Disorder: Abnormalities of Hemispheric Dominance

What have studies of people without depression found?

A

-a fairly strong relationship between happy mood and increased activity in the left prefrontal cortex

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26
Q

14.2 Antidepressant Drugs: Types of Antidepressants

List the antidepressant drugs in the textbook. (5)

A

-tricyclics
-selective serotonin reuptake inhibitors
-serotonin noreprinephrine reuptake inhibitors (SNRIs)
-monoamine oxidase inhibitors
-atypical antidepressants

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27
Q

14.2 Antidepressant Drugs: Types of Antidepressants

Describe Tricyclics. What is the mechanism? What are the effects? What are the side effects? What is its usage? What is an example of this? (5)

A

Mechanism: block reuptake of serotonin, dopamine and norepinephrine by inhibiting transporter proteins
Effects: Prolong NT presence in synaptic cleft.
Side Effects: drowsiness (blocks histamine receptors), dry mouth, difficulty urinating (blocks acetylcholine), heat irregularities (blocks sodium channels)
Usage: Limited due to its side effects
Example: Imipramine (Tofranil)

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28
Q

14.2 Antidepressant Drugs: Types of Antidepressants

Describe Selective Serotonin Reuptake Inhibitors (SSRIs). What is the mechanism? What are the effects? What are the side effects? What is its effectiveness? What is an example of this? (5)

-Compare side effects and effectiveness ti tricyclics

A

Mechanism: Blocks reuptake of serotonin by locking the transporter protein.
Effects: Increase serotonin levels in synaptic cleft
Side effects: Milder compared to Tricyclics
Effectiveness: Similar to tricyclics
Examples: Fluoxetine (Prozac), Sertraline (Zoloft), Fluvoxamine (Luvox), Citalopram (Celexa), Paroxetine (Paxil)

29
Q

14.2 Antidepressant Drugs: Types of Antidepressants

Describe serotonin norepinephrine reuptake inhibitors (SNRIs). What is the mechanism? What is the effect? What are examples? (3)

A

-Block reuptake of both serotonin and norepinephrine
-effects include improved mood and memory
examples: Duloxetine (Cymbalta), Venlafaxine (Effexor)

30
Q

14.2 Antidepressant Drugs: Types of Antidepressants

Describe monoamine oxidase inhibitors (MAOIs). What is their mechanism? What about the effects? What about side effects? Usage? Examples? (5)

A

-Block monoamine oxidase enzyme, preventing breakdown of catecholamines and serotonin
Effects: increase avaiulable NT levels
Side effects: dietary restrictions
Usage: Not first choice cause of dietary restrictions
Example: Phenelzine (Nardil)

31
Q

14.2 Antidepressant Drugs: Types of Antidepressants

Describe atypical antidepressants. What is an example? Mechanisms? Effectiveness? (3)

A

Example: Bupropion (Wellbutrin)
Mechanism: inhibits reuptake of dopamine and norepinephrine
Effectiveness: Comparable to other antidepressants

32
Q

14.2 Antidepressant Drugs: Types of Antidepressants

Describe two new possibilities for antidepressant drugs. (2)

A

-ketamine
-St. John’s Wort

33
Q

14.2 Antidepressant Drugs: How are antidepressants effective?

Describe the initial assumption and current understanding of why antidepressants are effective? (2)

A

Initial assumption: depression was thought to be caused by a deficiency in serotonin or other NT
Current Understanding: people with depression generally have normal levels of NT. Increasing serotonin levels doesn’t necessarily alleviate depression.

-the delayed mood elevation of antidepressants also didn’t work theoretically with the belief that depression was from a lack of serotonin, as the antidepressants increase serotonin levels in minutes or hours

34
Q

14.2 Antidepressant Drugs: How are antidepressants effective?

Describe the neurotrophin hypothesis to describe how antidepressants elevate mood. Why BDNF? What is it crucial for? What is low BDNF linked to? How do antidepressants interact with it? (4)

A

-people with depression often have low brain-derived neurotrophic factor
-BDNF is crucial for synaptic plasticity, learning and neuron growth
-low BDNF is linked to a smaller hippocampus, impaired learning and reduced new neuron production
-antidepressants may increase BDNF levels over weeks

35
Q

14.2 Antidepressant Drugs: How effective are antidepressants

How effective are antidepressant drugs? What severity of depression are they most effective for? What are the limitations? (3)

A

-antidepressants are generally more effective than placebos, but the difference is small
-most effective for severe depression
-some studies may understate effectiveness due to low doses or less reliable depression scales

-research goes both ways essentially

36
Q

14.2 Antidepressant Drugs: Alternatives to antidepressant drugs

What is an advantage of psychotherapy over antidepressant drugs? (2)

A

-People who respond well to psychotherapy have a lower risk of later relapse than people who respond to antidepressant drugs.
-Also, antidepressant drugs produce unpleasant side effects.

37
Q

14.2 Antidepressant Drugs: Alternatives: Electroconvulsive therapy

What is electroconvulsive therapy? How effective is it for depression? What are drawbacks? (3)

A

-an electrically induced seizure
-it is effective in most cases of people with severe depression
-memory impairment and the effects don’t last long

-ECT increases the proliferation of new neurons in the hippocampus

38
Q

14.2 Antidepressant Drugs: Exercise and Diet

How does moderate-intensity exercise affect depression?

A

-moderate antidepressant benefits, especially for people over 60

39
Q

14.2 Antidepressant Drugs: Exercise and diet: Altered sleep patterns

What change in sleep habits sometimes relieves depression?

A

-Going to bed earlier sometimes relieves depression.

40
Q

14.2 Antidepressant Drugs: Exercise and diet: Altered sleep patterns

What are the advantages of bright-light treatment compared to antidepressant drugs?

A
  • It is cheaper, has little risk of side effects, and produces its benefits more quickly.
41
Q

14.2 Antidepressant Drugs: Exercise and diet: Deep brain stimulation

What is deep brain stimulation? How effective is it for depression? (2)

A

-a physician implants battery-powered device into the brain to deliver periodic stimulation to certain brain areas
-in the early stages, but results have been encouraging

42
Q

14.2 Bipolar Disorder

What are the two types of depression? Describe them briefly. (2)

A

-unipolar, people vary between normality and depression
-bipolar, alternate between depression and mania

-some people have full-fledged manic episodes know as bipolar 1 and other have mild or hypomanic episodes known as bipolar 2

43
Q

14.2 Bipolar Disorder

What is Mania?

A

-restless activity, excitement, laughter, excessive self-confidence, rambling speech, and loss of inhibitions

44
Q

14.2 Bipolar Disorder: Treatments

What are common treatments for bipolar disorder? (2)

A

-The common pharmaceutical treatments for bipolar disorder are lithium salts and certain anticonvulsant drugs—valproate and carbamazepine.
-A diet that includes omega-3 fatty acids also helps, as does a consistent sleep schedule.

45
Q

14.3 Schizophrenia: Diagnosis

What did Bleuler mean when he named Schizophrenia? What is the DSM diagnose for it? What are the symptoms? (3)

A

-he saw a split between the person’s emotional expression and intellectual experiences
-they must have deteriorated in everyday functioning for at least 6 months and the person must have some of these symptoms:
Symptoms:
-delusions: unjustifiable beliefs such as being controlled by aliens
-hallucinations: false sensory experiences
-disorganized speech
-grossly disorganized behavior
-weak emotional expression, speech and socialization

-belief that working memory may relate to schizophrenia

46
Q

14.3 Schizophrenia: Diagnosis

What are positive symptoms? What are negative symptoms? (2)

A

-positive symptoms are behviors that should be absent like hallucinations
-negative symptoms are behaviors that are not present but should be like emotional expression or socialization

47
Q

14.3 Schizophrenia: Diagnosis: Differential Diagnosis of Schizophrenia

What is a differential diagnosis?

A

-to diagnose schizophrenia in someone, a therapist must rule out other options first

48
Q

14.3 Schizophrenia: Diagnosis: Differential Diagnosis of Schizophrenia

What are the other options therapists must rule out to diagnose schizophrenia?

A

-substance abuse, brain damage, undetected hearing deficits, Hungtington’s disease, nutritional problems

49
Q

14.3 Schizophrenia: Genetics: Family Studies

What do monozygotic twins have when it comes to schizophrenia compared to dizygotic twins? What does this suggest? (2)

A

-a higher concordance (agreement) for schizophrenia about 50%
-could suggest a genetic influence

50
Q

14.3 Schizophrenia: Genetics: Family Studies

What are the limitations to the high concordance of monozygotic twins for schizophrenia? (2)

A

-monozygotic twins have only about 50% concordance, not 100%
-note the greater similarity between dizygotic twins than between siblings. Dizygotic twins have the same genetic resemblance as siblings but greater environmental similarity, including prenatal environment.

51
Q

14.3 Schizophrenia: Genetics: Adopted Children who develop schizophrenia

Discuss how research on adopted children supports a strong genetic basis for schizophrenia, but has limitations.

A

-for adopted children with shcizophrenia, the disorder is more common in their biological relatives than their adopting relatives, suggesting genetic but also prenatal influence as the time the child spent with the mother will influence them still

52
Q

14.3 Schizophrenia: Genetics: Efforts to locate a gene

Do any common genes produce a notable increase in the probability of schizophrenia? Why or why not? (2)

A

-nothing that produces more than a small increase
-people with schizophrenia have less children

53
Q

14.3 Schizophrenia: Genetics: Efforts to locate a gene

What does gene DISC1 control? How does it relate to people with schizophrenia? (5)

A

Controls:
-differentiation and migration of neurons in brain development
-production of dendritic spines
-generation of new neurons in the hippocampus
-learning
Relates to diagnosis:
-variants in this gene are more common in people with schizophrenia

54
Q

14.3 Schizophrenia: The Neurodevelopmental Hypothesis

What is the neurodevelopmental hypothesis? What three pieces of evidence support it? (4)

A

Definition: prenatal or neonatal influences produce abnormalities in the developing brain which can leave it vulnerable to schizophrenia
Evidence:
-several kinds of prenatal or early difficulties are linked to later schizophrenia
-people with schizophrenia have minor brain abnormalities that apparently originate early in life
-it is plausible that early developmnental issues could impair behavior in adulthood

55
Q

14.3 Schizophrenia: The Neurodevelopmental Hypothesis: Prenatal and Neon

Torrey and colleagues identified environmental factors that were intermediate and low risk factors for schizophrenia in children. List the intermediate environmental risk factors. (2)

-no high risk factors were identified

A

-living in a crowded city
-prenatal or childhood infection with toxoplasma gondii (cat poop)

56
Q

14.3 Schizophrenia: The Neurodevelopmental Hypothesis: Prenatal and Neon

Torrey and colleagues identified environmental factors that were intermediate and low risk factors for schizophrenia in children. List the low environmental risk factors. (6)

-no high risk factors were found

A

-poor nutrition of mom during pregnancy, premature birth, low birth weight and complications during delivery
-mom exposed to extreme stress
-head injuries in childhood
-acute infections in childhood
-Rh incompatibility
-season-of-birth effect: the tendency for people born in winter t have a slightly greater probability of developing schizophrenia

57
Q

14.3 Schizophrenia: The Neurodevelopmental hypothesis: Mild Brain Abnorm

Describe the important brain abnormalities of people with schizophrenia. (2)

A

-many, but not all, people with shcizophrenia show mild variable abnormalities of brain anatomy including less than average gray matter, especially in the hippocampus, amygdala and thalamus
-dorsolateral prefrontal cortex, show difficulty shifting to new rules in a card game

58
Q

14.3 Schizophrenia: Treatments: Antipsychotic drugs and dopamine

What are the two classes of antipsychotic drugs used for schizophrenia? What do they do? (3)

A

-phenothiazines
-butyrophenones
-they block dopamine synapses (D2 synapses)

59
Q

14.3 Schizophrenia: Treatments: Antipsychotic drugs and dopamine

What is the dopamine hypothesis of schizophrenia? Where in the brain? (2)

A

-schizophrenia results from excess activity at dopamine synapses in certain brain areas
-basal ganglia

60
Q

14.3 Schizophrenia: Treatments: Antipsychotic drugs and dopamine

What evidence supports the dopamine hypothesis of schizophrenia?

A

-in someone with schizophrenia, the concentration of dopamine in the brain as a whole is no higher than normal, dopamine released is increased in the basal ganglia
-extensive abuse of drugs which increase dopamine at the synapes induces substance-induced psychotic disorder

-study found people with schizophrenia had about twice as many D2 receptors occupied as normal

61
Q

14.3 Schizophrenia: Treatments: Second-generation antipsychotic drugs

What is the mesolimbocortical system? Which drugs produce their benefits by acting on neurons in this system? (2)

A

-neurons that project from the midbrain to the limbic system and prefrontal cortex
-drugs that block dopamine synapses

62
Q

14.3 Schizophrenia: Treatments: Second-generation antipsychotic drugs

Besides the mesolimbocortical system, where else do antipsychotic drugs block dopamine neurons? What is the side effect of this? (2)

A

-in the mesostriatal system that projects to the basal ganglia
-side effect is tardive dyskinesia (tremors)

63
Q

14.3 Schizophrenia: Treatments: Second-generation antipsychotic drugs

What are second-generation antipsychotics trying to do? What are cons? (2)

A

-reduce the risk of tardive dyskinesia
-other side effects though

64
Q

14.3 Schizophrenia: Treatments: Role of glutamate

What is the glutamate hypothesis of schizophrenia?

A

-part of the problem is the deficient activity at glutamate synapses in the prefrontal cortex

65
Q
A
66
Q

14.3 Schizophrenia: Treatments: Role of glutamate

What is evidence that supports the glutamate hypothesis of schizophrenia?

A

-studies have found decreased glutamate in the prefrontal cortex for schizophrenic people
-the effects of phencyclidine (PCP) a drug that inhibits NMDA glutamate receptors produces symptoms like schizophrenia

67
Q

14.4: Autism: Symtoms and Characteristics

What are the characteristics of autism spectrum disorder? (5)

A

-deficits in social and emotional exchange
-deficits in gestures, facial expressions and other nonverbal communication
-stereotyped behaviors, such as reptitive movements
-resistance to a change in routine
-unsually weak or strong responses to stimuli

68
Q

14.4: Autism: Genetics and other causes

Describe some of the causes of autism disucssed in the textbook. (5)

A

-many genes have been linked to autism, but no common gene exerts a large effect
-older fathers
-mother exposed to pesticides, solvents, perfumes or air pollutants during pregnancy
-certain antibodies
-lack of folic acid