Pharmacological and Neurobiological Approaches to Clinical and Health Psychology
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Pharmacological and Neurobiological Approaches to Clinical and Health Psychology - Complete Course Summary
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Pharmacological and Neurobiological Approaches to Clinical and Health Psychology
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Universiteit Leiden (UL)
Book
Psychopharmacology
Very compact notes (yet comprehensive in detail), for the elective exam of Pharmacological and Neurobiological Approaches to Clinical and Health Psychology. Includes all the material from the lectures, completed with each article and book chapter of the week. Contains at the end a short glossary of...
pharmacological and neurobiological approaches to clinical and health psychology
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Main Topics Notes
Lec 1 - Introduction - genetic sensitivity RA & depression, structural brain changes, immune system, serotonin &
depression → an interaction between processes, multidimensional intervention
application - allergy: early manifestation of immune dysregulation, classic psychosomatic disorder, complex
interactions, socially relevant; higher rate within families (35-75% genes), environ: too quick
incidence to be evolution alone, influence of stress, epigenetics processes: immune cell
differentiation & regulation; time window & dose influences, heterogeneous
- schizophrenia: heritability gap (twin studies overestimate heredity bc also share environ;
(20-35% genes)
Down's: 100% genes; MDD: 20-25% genes (a er correction for shared environ)
- clinical: change environ; Crisp-CAS9 changes DNA and alters epigenetics in many ways
How to Use an Article - pharmacogenomics = genetics to improve diagnosis and therapy
about Genetic Association - pedigree = diagram w/ heritable traits across 2+ generations of a family
- allele = variant of a gene; haplotype = alleles occurring together bc SNPs are close (so are
inherited together = genetic linkage); variant allele = the last frequent one (VS wild-type allele)
- cell → nucleus → chromosomes (22 pairs + 1 sex, winded by histones = proteins, to fit) → DNA
(bars are sugar-phosphate) → genes (a sequence of letters that encode for protein: adenine,
thymine, guanine, cytosine; each base pair is a rung; nucleotide = 1 base + phosphate groups; starts
w/ promotor, ends with terminator region)
- genome: DNA set of a human, 23 chromosomes egg + 23 chromosomes sperm
- phenotype: GxE, outward charac, personality (outside gene), genotype: genetic make-up
- SNPs = single-nucleotide polymorphism (single base pair change, vs common sequence);
synonymous SNP = SNP does not lead to change in amino acid
- VNTRs = variable number of tandem repeats
- epigenome: what is actually activated/ deactivated, some inprints survive through generations,
is changeable, depends on timing, changes constantly throughout the day!;
- epigenetics: without changes in DNA sequence, biochemical processes that switch genes
on/off, triggered by environ factors, signals come from the inside cell, nearby cells, and exterior;
modifies histones and accessibility to DNA transcription
- isoform = variant in amino acid sequence of a protein, the different proteins
Mechanisms of Genetics - gene to protein: DNA is transcribed into mRNA (messenger ribonucleic acid) → mRNA translated
into protein, in the ribosome (protein synthesis machinery, outside nucleus); first it's unwinded
genetic variation - >99% of DNA is similar across humans, <1% differs across individuals
- mutations = rare permanent change in base (deletion/ duplication/ DNA not repaired), <1%
- polymorphisms = 2+ variants of a gene (allele) occurring w/ at least 1% of the less common
variant; transmitted through generations, no major defect in bio functions: 1) presence/ deletion
of a stretch of DNA (involves DNA duplication = copy number variation = CNV); 2) repeating
patterns of DNA; 3) single-base pair change (SNPs), may be from segment that codes for protein,
or just influence cell function, the most common
- e.g. APOE gene: 3 alleles = e2, e3 (most common in white population), e4; additive model
- Models of Inheritance: 1) dominant (in hetero vs homozygous); 2) recessive (if heterozygote,
allele remains biologically silent - only in genotype -, does not produce protein); 3) additive =
allele increases trait proportionately; 2 differing proteins from different alleles share function (=
per-allele model) → epistasis = interaction of genes
Hardy-Weinberg - for 2 alleles (A, frequency p; and a, frequency q), a er 1 generation of random mating, the
Equilibrium genotype frequencies of AA, Aa and aa in the population will be pˆ2, 2pq, qˆ2; [p + q = 1] and [pˆ2
+ 2pq + qˆ2 = 1]
- deviations from HWE may be explained by: 1) inbreeding (not random mating); genetic dri
(population is limited and isolated); 3) migration; 4) new mutations (rare, bc in sufficiently large
population, 1 generation is enough to reach equilibrium); 5) selection (disadvantage for an allele,
e.g. leading to fetal death); or methodological problems with the genetic study itself
- pedigree studies: good for rare disease caused by rare mutation
Genetic Association Studies - candidate gene study: testing a priori hypothesis that specific genes (also with low allele
frequency) are associated with disease; hypothesis-driven VS
- genome-wide association study: test over 1 million genetic variants that are frequent in the
population (SNPs); needs large sample size; agnostic, needs replication studies to check for
spurious associations;
, - the 2 methods are not mutually exclusive; usually represent population-based investigations
((non)diseased are unrelated); or in family members with mutations (linkage analysis); variation to
a gene is linked to an outcome
Linkage Disequilibrium = nearby stretches of a genome (tend to be) inherited together as a unit, result in hyplotype
blocks; → makes it hard to know whether the specific SNP has causal correlation (that's
important for therapeutic interventions, but not necessarily for determining risk)
- in genetic association studies, one goal may be to determine whether SNP is causally
associated with outcome
GxE & Psychiatric - nature/ heredity vs nurture/ environment: inseparable, mostly result of interaction → 37% MDD,
Disorders 65-80% schizophrenia, 60-85% bipolar
candidate GxE studies - most studied: serotonin transporter, MAOA, dopamine receptor DRD4 and DRD2, COMT, and
BDNF (brain-derived neurotrophic factors); are associated w/ multiple disorders (comorbidity)
- 5-HTTLPR & depression: serotonin transporter; s-allele is for less serotonin transporter mRNA
transcription, moderates serotonergic response to stress, makes a difference if exposed to
maltreatment/ stress → + suicidality and depression; still not clear (some show no effect); also
BDNF x SLEs → matches monoamine hypothesis (serotonins, antidepressants ↑ these levels)
- MAOA & antisocial behavior: codes for monoamine oxidase A, breaks NTs; short allele → low
MAOA expression → higher NTs; short allele + traumatic childhood; overall consistent support,
but also moderated by gender (stronger in boys)
- COMT & schizophrenia: codes for enzyme that degrades catecholamine NTs; valine allele = +
dopamine degradation; Val allele (but not Met) + cannabis use → psychotic symptoms; Met allele
+ stress → psychosis (but only for clinical patients); but inconsistent results (study designs?)
- GABA-receptor & alcohol dependence: x lower parental monitoring/ peer group antisocial &
substance availability; antagonists of GABA-receptor are effective in treatment of dependence
- Diathesis-Stress: environ only leads to psychop. when w/ inherent (genetic, temperament)
vulnerability; if not vulnerable (or counterbalanced w/ protective factors) = resilient
- alternative: differential susceptibility = Diathesis-Stress (+ negative exposure = for worse) &
Vantage Sensitivity (+ positive exposure = for better) → resilience as in Diathesis-Stress = "low
susceptibility to environmental influence" and vulnerability = "high susceptibility" - it's about genetic
sensitivity rather than vulnerability, studies should also cover the positive influence of environ
- it's evolutionary-inspired: the gene variants have survived natural selection, so must provide
benefits that counteract negative effects of heightened vulnerability
- but not necessarily always environmental sensitivity, sometimes it's just vulnerability
- limitations of candidate GxE studies: requires strong biological hypothesis, but only so much
is known, so a publication bias and wrong gene candidates; behaviors are rather polygenic;
difficult to replicate findings (small sample size, false positives?; most have been conducted
from Diathesis-Stress model perspective → shi ing to genome-wide
genome-wide association - hypothesis-free, threshold for statistical significance is very high; SNP-based heritability
studies (GWAS) estimates are a lot lower than in twin-studies (e.g. 20% vs 80%) - does not include GxE →
discrepancies in studies!
- genome-wide environment interaction studies (GWEIS): only a few so far, needs even larger
sample size!, more statistically complex; tests G and GxE associations on outcomes (SNP by
SNP approach to GxE)
- polygenic score-X-environment interaction studies: test interaction btw polygenic score (PGS)
& environmental variable; e.g. effects of childhood trauma in MDD was greater for those with
higher PGS for MDD (but unclear); → do more longitudinal studies!!; do + extensive, objective
measures of environ
future directions - obtain better environ measures: more accurate, avoid self-reports; experience sampling method
(ESM) = less recall bias, mood effect, App; consider multiple factors: childhood maltreatment,
season of birth, vitamin D, urbanicity, minority status, SES, cannabis use, SLEs in adulthood
- focus on transdiagnostic phenotypes: effects of GxE are transdiagnostic, comorbidity,
multifinality; e.g. 5-HTTLPR S-allele + daily stress → development of transdiagnostic emotion
dysregulation phenotype (no specific psychiatric disorder)
- developmental perspective: GxE depends on timing (more in childhood), do life course study
(gene-x-environ in childhood-x-environ in adulthood)
- new analytical approaches & study designs: not necessarily mutually exclusive, first consider
type of GxE, then the manner it operates
- focus on vulnerability genes (showing effect in GxE), instead of multiple-testing with all others
- for differential susceptibility genes, use MZ twins, see their difference (from non-shared
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