2. Two or more of the following symptoms:
Delusions
Hallucinations
Disorganized speech (e.g frequent derailment or incoherence
Grossly disorganized or catatonic behavior
Negative symptoms (alogia, avolition, affective flattening).
Social/occupational dysfunction
Duration: at least 6months
3. Episodic With Interepisode Residual
Symptoms
Episodic with no Interepisode Residual
Symptoms
Single episode in Partial Remission
Single Episode in Full Remission
Other Unspecified Pattern
4. Paranoid Type
Disorganized Type
Catatonic Type
Undifferentiated Type
Residual Type
6. A single abnormal gene expresses an abnormal product, with
the consequence of causing an inherited disease in a classic
autosomal dominant manner.
7.
8. According to this theory, single abnormal
gene can also cause a mental illness.
An abnormal gene would produce an
abnormal gene product, which in turn would
lead to neuronal malfunction that directly
causes a mental illness.
No such gene has been identified, and there
is no longer any expectation that such a
discovery might be made.
9.
10. This theory postulates that, rather than genes
causing mental illness, genes instead cause
individual symptoms, behaviors, personalities or
temperaments.
According to this theory an abnormal gene
encoding for a symptom, behavior or trait would
cause neuronal malfunction leading to that
symptom, behavior or trait.
No genes for behaviors or personality have been
identified and there is no longer an expectation
that such a discovery might be made.
11.
12. Genes do not encode for mental illnesses, behaviors or
personalities. Genes encode for proteins.
Genes may produce genetically altered proteins that code for
subtle molecular abnormalities, which in turn may be linked to
the development of psychiatric symptoms.
Genes may code for an abnormality in the:
neuro-developmental process
synthesis or activity of enzymes
Transporter proteins
receptors
components of signal transduction
synaptic plasticity machinery and other neuronal components.
Each subtle molecular abnormality may convey risk for the
development of mental illness rather than directly causing a
mental illness.
13.
14. There is no gene for schizophrenia, bipolar
disorder, depression or anxiety and there will never
be one.
Genes do not code for psychiatric illnesses or for
symptoms of psychiatric illnesses.
Genes operate at a very basic cellular level. They code
for molecules and cells such as neuronal
cytoskeleton, neuronal migration
proteins, myelin, cellular adhesion molecules, and
dendritic cone growth.
Genes do not respect the boundaries of psychiatric
disorders. For instance most risk genes for
schizophrenia are present also in bipolar
disorder, schizoaffective disorder, Alzheimer’s
disease and anxiety.
15. More than a dozen genes have been
identified that increase the risk for
schizophrenia.
16.
17. Is regulated by four genes:
BDNF, Dysbindin, DISC 1 and neuregulin.
18.
19.
20.
21. Once nurture seemed clearly distinct from nature. Now it
appears that our diets and lifestyles can change the
expression of our genes. How? By influencing a network of
chemical switches within our cells collectively known as
the epigenom.
This new understanding may lead us to potent new
medical therapies.
Epigenetic cancer therapy, for one, already seems to be
yielding promising results.
Epigenetic treatment of mental illness is just around the
corner.
22. An Epigenome consists of a record of the
chemical changes to the DNA and
histone proteins of an organism.
These changes can be passed down to offspring.
23. For the most part, every cell in our body
contains exactly the same genes, but inside
the individual cells some genes are activated
while others are silenced.
When genes are active they are capable of
being translated into proteins. When genes
are silent, they are inaccessible for translation
into proteins.
24. Epigenomics is the science of activating or silencing genes at
the level of transcription or translation.
25. Genes can be activated or silenced :
-By modifying the histone proteins (H3 or H4)
-By modifying the DNA (methylation at CpG promoters)
-By small interfering RNAs
26.
27.
28.
29.
30.
31. Studies the biological substrate underlying
cognition.
A branch of physiology and neuroscience
brain networks:
1. think(cognition)
2. emotion (meaning)
3. motivation (goals)
33. Advances in microscopy, stem cells and imaging:
150 billion neurons
Each neuron up to 900 synapses
Number of connections - trillions
Connections organized in hubs
and networks
34. The salience network initiates dynamic switching between the central-
executive and default-mode networks, and mediates between attention to
endogenous and exogenous events.
Large Scale Brain Networks in Cognition, emerging methods and principles;Steven Bresler, Vinod Menon;
Trends in cognitive science, Vol 14,June 2010, pages277-290;
http://dx.doi.org/10.1016/j.tics2010 .04.004
