1. .

3. Schizophrenia; crash course psychology
What is schizophrenia?

7. The biology behind schizophrenia
Neuroleptics and antipsychotic drugs

9. Impact (symptoms) of schizophrenia
The future of schizophrenia treatment

12. 6 MUST KNOW SIGNS of DEPRESSION!

13. The science of depression

14. Depression is a disease of civilization: Stephen Ilardi at TEDxEmory

17. Depressive and Bipolar Disorders: Crash Course Psychology #30
5 misunderstandings about Bipolar Disorder - Mental Health Help with Kati Morton

24. Daniel My Brother (Huntington's Disease)

25. 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?

29. Tourette’s syndrome

34. Parkinson’s disease

45. Parkinson genes

46. 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.

47. 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.

53. Neurofibrillary Tangles (NFTs) are aggregates of hyperphosphorylated tau protein that are most commonly known as a primary marker of Alzheimer's Disease

64. Alzheimer's disease is a synaptic failure
DJ Selkoe - Science, 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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67. (a) Hypothetical relationship between Aβ level and synaptic activity
(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.