Hello there,

Please help me with this assignment. Please ensure there are at least 4 sentences in a paragraph and always cite the resources (preferably within the past 5 years). I have included some References that you could possibly use along with this week’s Lecture Note & a couple of articles.

 

1.Consider the neurobiology of our most basic drives. How do substance-abuse disorders most notably interfere with these basic human drives and the areas of the brain that control them? Support your position.

 

2.What does it mean to be "normal" or "abnormal," and to what extent does your place in a given culture at a moment in history influence this? Support your position.

 

3.Given what you have learned about biological psychology, how does biological psychology fit with your dissertation research topic? [Reference is not required for this DQ] Remember my dissertation research topic is: What are Teachers' Perceptions of Inclusion Related to Special Education Students with Emotional Disabilities?

References

Cardwell, M. (2012). The other side of normal: How biology Is providing the clues to unlock the secrets of normal and abnormal behavior. Library Journal, 137(8), 90-91.

Eysenck, H. J. (1958). The continuity of abnormal and normal behavior. Psychological Bulletin, 55(6), 429-432. doi:10.1037/h0048574

Kalat, J. W. (2016). Biological psychology (12th ed.). Belmont, CA: Thomson Wadsworth.

Kapustin, S. (2015). An existential criterion for normal and abnormal personality in the works of Erich Fromm. Psychology in Russia: State of Art, 8,(2), 87-98. doi:10.11621/pir.2015.0208

Kapustin, S. (2015). An existential criterion for normal and abnormal personality in the works of Sigmund and Alfred Adler. Psychology in Russia: State of Art, 8,(3), 4-16. doi: 10.11621/pir.2015.0301 

Newlin, D. B., & Thomson, J. B. (1990). Alcohol challenge with sons of alcoholics: A critical review and analysis. Psychological Bulletin, 108(3), 383-402. doi:10.1037/0033-2909.108.3.383

Zuren, G.A., & Ashley, W.M. (2012). In quest of the meaning of normal and abnormal behavior. American Journal of Contemporary Research. 2 (9), 20-25. R

PAGES_DCNS 46_5.qxd:DCNS#45 9/09/10 9:39 Page 289 Tr a n s l a t i o n a l r e s e a r c h
Genetics in schizophrenia:
where are we and what next?
Arun K. Tiwari, PhD; Clement C. Zai, PhD; Daniel J. Müller, MD, PhD;
James L. Kennedy, MD S chizophrenia is a devastating psychiatric disease
that has a lifetime prevalence of approximately 1%
worldwide. It is characterized by the occurrence of delusions, hallucinations, disorganized speech, alterations in
drive and volition, impaired cognition, and mood symptoms.1 The importance of both environmental as well as
genetic factors in the development of this complex disorder has been demonstrated. Growing up in an urban
environment, immigration, cannabis usage, male gender
and perinatal events (hypoxia, maternal infection, stress,
and malnutrition) are associated with increased risk of
developing schizophrenia.1,2 Evidence from family, twin,
and adoption studies suggests a strong genetic component. A meta-analysis of twin studies estimated the heritability to be 81% (confidence interval 73% to 90%)3
and a recent Swedish study of more than 2 million families estimated it to be 64%.4 Of all the known risk factors
for schizophrenia, genetics is the single largest one. No
precise mode of inheritance is known, and less than one
third of patients with schizophrenia have a family history.
Elucidation of etiological factors remains the overwhelming challenge to schizophrenia researchers. In fact,
the most effective method for identification of genetic
risk factors for schizophrenia is not clear, and this has led
to a number of approaches, including epigenetics, being
adopted, in an attempt to clarify the genetic etiology.
Since the initial observation that schizophrenia has a
polygenic mode of inheritance and availability of polymorphic markers for genetic mapping, many attempts Understanding the genetic basis of schizophrenia continues to be major challenge. The research done during
the last two decades has provided several candidate
genes which unfortunately have not been consistently
replicated across or within a population. The recent
genome-wide association studies (GWAS) and copy number variation (CNV) studies have provided important evidence suggesting a role of both common and rare large
CNVs in schizophrenia genesis. The burden of rare copy
number variations appears to be increased in schizophrenia patients. A consistent observation among the
GWAS studies is the association with schizophrenia of
genetic markers in the major histocompatibility complex
(6p22.1)-containing genes including NOTCH4 and histone protein loci. Molecular genetic studies are also
demonstrating that there is more overlap between the
susceptibility genes for schizophrenia and bipolar disorder than previously suspected. In this review we summarize the major findings of the past decade and suggest areas of future research.
© 2010, LLS SAS Author affiliations: Neurogenetics section, Neuroscience department, Centre for
Addiction and Mental Health, Toronto, Ontario, Canada Dialogues Clin Neurosci. 2010;12:289-303. Keywords: schizophrenia; linkage; candidate gene; whole genome association
study, GWAS; copy number variation; CNV; common variant; rare variant Copyright © 2010 LLS SAS. All rights reserved Address for correspondence: James L Kennedy, R-30, Neurogenetics section, Center
for Addiction and Mental Health, 250 College Street, Toronto, Ontario, Canada M5T
1R8
(e-mail: James_Kennedy@camh.net) 289 www.dialogues-cns.org PAGES_DCNS 46_5.qxd:DCNS#45 9/09/10 9:39 Page 290 Tr a n s l a t i o n a l r e s e a r c h
have been made to find susceptibility genes for schizophrenia using either the methods of linkage or association.5,6
One of the early strategies used to begin unraveling the
genetic contribution of schizophrenia was the investigation of chromosomal aberrations and familial syndromes
with schizophrenia-like phenotypes. Chromosomal aberrations have been reported in families with schizophrenia and other psychiatric disorders.7,8 The deletion of a
section of 22q11 leads to the phenotype of velocardiofacial (DiGeorge) syndrome that includes abnormalities
in facial features, the palate, and midline heart defects.
Gene
AKT1
APOE
COMT Patients with 22q11 deletion syndrome exhibit psychotic
symptoms resembling schizophrenia at a frequency of
18%, a rate that is much higher than the overall 1%
prevalence of schizophrenia in the general population.
On the other hand, when focusing on populations of
patients who have the diagnosis of schizophrenia, at least
2% of these individuals are reported to have 22q11 deletions compared with the 0.025% prevalence in the general population.9,10 This region of 22q11 harbours the
COMT and PRODH genes among others

Attachments:

• 1506698851-GCU PSY 847 Biological Psychology Lecture 7.docx
• 1506698874-GCU PSY 847 Alcohol Challenge With Sons of Alcoholics.A Critical Review and Analysis.pdf
• 1506699030-GCU PSY 847.Genetics in Schizophrenia where are we and what next.pdf