Transcript PowerPoint 프레젠테이션

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Schizophrenia; crash course psychology
http://www.youtube.com/watch?v=uxktavpRdzU
What is schizophrenia?
http://www.youtube.com/watch?v=ynin-1yAERY
The biology behind schizophrenia
http://www.youtube.com/watch?v=V1kSIfxBVfU
Neuroleptics and antipsychotic drugs
http://www.youtube.com/watch?v=aGfNBDXYs1Y
Impact (symptoms) of schizophrenia
http://www.youtube.com/watch?v=su
VEMf9anzE
The future of schizophrenia treatment
http://www.youtube.com/watch?v=bsah3K6js8
6 MUST KNOW SIGNS of DEPRESSION!
http://www.youtube.com/watch?v=51vdnwrfsNA
The science of depression
http://www.youtube.com/watch?v=GOK1tKFFIQI
Depression is a disease of civilization: Stephen Ilardi at TEDxEmory
http://www.youtube.com/watch?v=drv3BP0Fdi8
Depressive and Bipolar Disorders: Crash Course Psychology #30
http://www.youtube.com/watch?v=ZwMlHkWKDwM
5 misunderstandings about Bipolar Disorder - Mental Health Help with Kati Morton
http://www.youtube.com/watch?v=oUI5xS_IH24
Daniel My Brother (Huntington's Disease)
http://www.youtube.com/watch?v=JzAPh2v-SCQ
The Huntingtin gene provides the genetic information for a
protein that is also called "huntingtin". Expansion of a CAG
triplet repeat stretch within the Huntingtin gene results in a
different (mutant) form of the protein, which gradually damages
cells in the brain, through mechanisms that are not fully
understood.
What is Huntington's Disease?
http://www.youtube.com/watch?v=4HgFUvVyHYQ
Tourette’s syndrome
http://www.youtube.com/watch?v=jYRa-fpNonY
Parkinson’s disease
http://www.youtube.com/watch?v=wWQoLEKq4Wc
Parkinson genes
Nature Editor's summaryin‫العر‬
Loss-of-function mutations affecting two
enzymes involved in the clearance of damaged
mitochondria (mitophagy) — the ubiquitin
ligase parkin and the protein kinase PINK1 —
are associated with familial Parkinson's disease.
Here it is shown that USP30, a deubiquitinase
localized to mitochondria, antagonizes
mitophagy by removing the ubiquitin tags put
in place by parkin. Reducing USP30 activity
enhances mitochondrial degradation in
neurons, and knockdown of USP30 rescues
defective mitophagy caused by pathogenic
mutations in parkin. Knockdown of USP30 in
aDrosophila model improves mitochondrial
integrity and survival in both parkin- and
PINK1- deficient flies. Thus, USP30 inhibition is
potentially beneficial for Parkinson's disease by
promoting mitochondrial clearance and quality
control.
A graphical representation of how cellular health can be affected by changes in the levels of
mitophagy — the process by which cells dispose of mitochondria that have become defective
or damaged. Insufficient or excessive mitophagy reduces cellular health, owing to
accumulation of defective mitochondria or disposal of too many mitochondria, respectively.
PINK1–parkin signalling promotes mitophagy, and Bingol et al.1 now find that an enzyme,
USP30, opposes the action of the parkin enzyme and inhibits mitophagy (not shown). Thus,
in cells that express both parkin and USP30, a balanced level of mitophagy is maintained.
Neurofibrillary Tangles (NFTs) are aggregates
of hyperphosphorylated tau protein that are
most commonly known as a primary marker of
Alzheimer's Disease
Alzheimer's disease is a synaptic failure
DJ Selkoe - Science, 2002 - sciencemag.org
Abstract In its earliest clinical phase, Alzheimer's disease characteristically produces a
remarkably pure impairment of memory. Mounting evidence suggests that this
syndrome
begins with subtle alterations of hippocampal synaptic efficacy prior to frank
neuronal ...
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(a) Hypothetical relationship between Aβ level and synaptic activity. Intermediate levels of
Aβ enhance synaptic activity presynaptically, whereas abnormally high or low levels of Aβ
impair synaptic activity by inducing postsynaptic depression or reducing presynaptic
efficacy, respectively. (b) Within a physiological range, small increases in Aβ primarily
facilitate presynaptic functions, resulting in synaptic potentiation38, 39. (c) At abnormally
high levels, Aβ enhances LTD-related mechanisms, resulting in postsynaptic depression and
loss of dendritic spines4, 7, 31, 46.