Schizophrenia crash course psychology http www youtube comwatch

Schizophrenia; crash course psychology http: //www. youtube. com/watch? v=uxktavp. Rdz. U What is schizophrenia? http: //www. youtube. com/watch? v=ynin-1 y. AERY Schizophrenia - causes, symptoms, diagnosis, treatment & pathology https: //www. youtube. com/wa tch? v=PURv. JV 2 SMso

The biology behind schizophrenia http: //www. youtube. com/watch? v=V 1 k. SIfx. BVf. U Neuroleptics and antipsychotic drugs http: //www. youtube. com/watch? v=a. Gf. NBDXYs 1 Y

Impact (symptoms) of schizophrenia http: //www. youtube. com/watch? v=su VEMf 9 anz. E The future of schizophrenia treatment http: //www. youtube. com/watch? v=bsah 3 K 6 js 8

Figure 1: Progress in identifying schizophrenia-associated genes. Since 2009, genome-wide analyses of the genetic loci associated with schizophrenia (including the current study by the Schizophrenia Working Group of the Psychiatric Genomics Consortium 1, labelled 2014) have yielded increasing numbers of 'hits'1, 9, 15, 16. Over this time, there has been a correlation between the number of people tested and the number of susceptibility-associated loci found.

Nature Article Biological insights from 108 schizophreniaassociated genetic loci • Schizophrenia Working Group of the Psychiatric Genomics Consortium Biological insights from 108 schizophrenia-associated genetic loci Schizophrenia Working Group of the Psychiatric … - Nature, 2014 - nature. com Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genomewide association studies. Here we report a multi-stage schizophrenia genome-wide association 1831회 인용 관련 학술자료 전체 44개의 버전

Figure 1: Manhattan plot showing schizophrenia associations. Manhattan plot of the discovery genome-wide association meta-analysis of 49 case control samples (34, 241 cases and 45, 604 controls) and 3 family based association studies (1, 235 parent affected-offspring trios).

6 MUST KNOW SIGNS of DEPRESSION! http: //www. youtube. com/watch? v=51 vdnwrfs. NA

Animation: Depression and its treatment (from Nature) http: //www. nature. com/neuro/multimedia/depression/index. html The science of depression http: //www. youtube. com/watch? v=GOK 1 t. KFFIQI Clinical depression - major, post-partum, atypical, melancholic, persistent https: //www. youtube. com/watch? v=Qhuk. M 33 VLgo

Ketamine for resistant depression: Outstanding promise, outstanding issues. Posted on August 26, 2013 Outstanding Promise. Ketamine has been around for many years, firstly as a dissociative anaesthetic and then as a psychedelic drug. But it might become best known for it's powerful antidepressant properties (Berman et al 2000; Zarate et al 2006). Compared to existing antidepressants, which take around 2 weeks to work, ketamine exerts a large antidepressant effect on the first day of treatment. The robust antidepressant effect of ketamine also occurs in patients who have not found relief with existing drugs or with ECT.

Signaling Pathways Underlying the Rapid Antidepressant Actions of Ketamine Ronald S. Duman

Depression is a disease of civilization: Stephen Ilardi at TEDx. Emory http: //www. youtube. com/watch? v=drv 3 BP 0 Fdi 8

Bipolar disorder (depression & mania) - causes, symptoms, treatment & pathology https: //www. youtube. com/watch? v=KSvk 8 LLBo 2 g Depressive and Bipolar Disorders: Crash Course Psychology #30 http: //www. youtube. com/watch? v=Zw. Ml. Hk. WKDw. M 5 misunderstandings about Bipolar Disorder - Mental Health Help with Kati Morton http: //www. youtube. com/watch? v=o. UI 5 x. S_IH 24

Therapeutic Potential of Mood Stabilizers Lithium and Valproic Acid: Beyond Bipolar Disorder

A schematic illustration of the central hypothesis of molecular actions of mood stabilizers lithium and VPA. Through the inhibition of GSK-3 and HDACs, respectively, lithium and VPA are hypothesized to regulate the transcription and expression of factors critically involved in neuroprotective, neurotrophic, antiinflammatory, neurogenic and angiogenic, mood-stabilizing, antidepressant-like, and anxiolytic effects, in addition to regulating stem cell migration and mi. RNAs. The underlying mechanisms of these actions have been elucidated by both in vitro and in vivo experimental settings and are discussed in this review. Lines with solid arrows represent stimulatory connections; lines with flattened ends represent inhibitory connections. Dashed lines represent pathways with reduced activity as a result of drug treatment.

SHANK 3 overexpression causes manic-like behaviour with unique pharmacogenetic properties K Han, JL Holder Jr, CP Schaaf, H Lu, H Chen, H Kang… - Nature, 2013 - nature. com Mutations in SHANK 3 and large duplications of the region spanning SHANK 3 both cause a spectrum of neuropsychiatric disorders, indicating that proper SHANK 3 dosage is critical for normal brain function. However, SHANK 3 overexpression per se has not been established 154회 인용 관련 학술자료 전체 17개의 버전

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. Daniel My Brother (Huntington's Disease) http: //www. youtube. com/watch? v=Jz. APh 2 v-SCQ Huntington disease - causes, symptoms, diagnosis, treatment & pathology https: //www. youtube. com/watch? v=Iu. Sa. Xi. RVqg 0

Version 1. F 1000 Res. 2016; 5: F 1000 Faculty Rev-152. Published online 2016 Feb 9. doi: 10. 12688/f 1000 research. 7424. 1 PMCID: PMC 4755417 Recent Advances in Understanding and Managing Tourette Syndrome Mary Ann Thenganatt 1 and Joseph Jankovica, 1 While TS is clearly a familiar disorder, often with bilineal inheritance (both parents affected) 22, our understanding of the genetic underpinnings of TS is still in its infancy 23. A population-based study in Sweden found overall heritability of tic disorders to be 0. 77, increasing with the degree of genetic relatedness: odds ratio (OR) of first-degree relatives (18. 69) greater than that of second degree relatives (OR 4. 58), which was greater than that of third-degree relatives (OR 3. 07) 24. Despite the strong heritability of TS, a causative gene or genes have yet to be discovered 25. Various study designs have evaluated the genetics of TS including twin studies, linkage analyses, cytogenic abnormalities, copy number variation studies, and genome-wide association studies (GWAS) 23. Studies of multigenerational pedigrees of TS families have found an association between a functional mutation in the histamine decarboxylase ( HDC) gene and TS 26, 27. The HDC gene encodes for L-histidine decarboxylase, which is the rate-limiting step enzyme in histamine production. The first GWAS in TS included 1285 cases and 4964 controls of European ancestry 28. In the primary analysis, no markers achieved a genome-wide threshold of significance (p<5× 10 -8); the strongest signal was found in rs 7868992 on chromosome 9 q 32 within COL 27 A 1 (p=1. 85× 10 -6).

Tourette's syndrome & tic disorders - definition, symptoms, diagnosis, treatment https: //www. youtube. com/watch? v=1 w 8 l. POg. Fxt 4 Tourette's Syndrome - Life With Tourette's http: //www. youtube. com/watch? v=j. YRa-fp. Non. Y

Parkinson's disease - causes, symptoms, diagnosis, treatment & pathology https: //www. youtube. com/watch? v=VIEUEV 9 wly. I

Michael J Fox Parkinson's Disease https: //www. youtube. com/watch? v=ECk. PVTZlf. P 8 Dad Living With Parkinson's https: //www. youtube. com/watch? v=8 bp 9 n 60 m 3 A Y

Parkinson genes

Nature Editor's summaryin ﺍﻟﻌﺮ Loss-of-function mutations affecting two enzymes involved in the clearance of damaged mitochondria (mitophagy) — the ubiquitin ligase parkin and the protein kinase PINK 1 — are associated with familial Parkinson's disease. Here it is shown that USP 30, a deubiquitinase localized to mitochondria, antagonizes mitophagy by removing the ubiquitin tags put in place by parkin. Reducing USP 30 activity enhances mitochondrial degradation in neurons, and knockdown of USP 30 rescues defective mitophagy caused by pathogenic mutations in parkin. Knockdown of USP 30 in a Drosophila model improves mitochondrial integrity and survival in both parkin- and PINK 1 - deficient flies. Thus, USP 30 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. PINK 1–parkin signalling promotes mitophagy, and Bingol et al. 1 now find that an enzyme, USP 30, opposes the action of the parkin enzyme and inhibits mitophagy (not shown). Thus, in cells that express both parkin and USP 30, a balanced level of mitophagy is maintained.

Alzheimer's disease - plaques, tangles, causes, symptoms & pathology https: //www. youtube. com/watch? v=v 5 gd. H_Hydes

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. . . 3144회 인용

(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 potentiation 38, 39. (c) At abnormally high levels, Aβ enhances LTD-related mechanisms, resulting in postsynaptic depression and loss of dendritic spines 4, 7, 31, 46.

Cell. 2017 Jan 26; 168(3): 427 -441. e 21. doi: 10. 1016/j. cell. 2016. 12. 044. Epub 2017 Jan 19. Apo. E 2, Apo. E 3, and Apo. E 4 Differentially Stimulate APP Transcription and Aβ Secretion. Huang YA 1, Zhou B 2, Wernig M 3, Südhof TC 4. Author information Abstract Human apolipoprotein E (Apo. E) apolipoprotein is primarily expressed in three isoforms (Apo. E 2, Apo. E 3, and Apo. E 4) that differ only by two residues. Apo. E 4 constitutes the most important genetic risk factor for Alzheimer's disease (AD), Apo. E 3 is neutral, and Apo. E 2 is protective. How Apo. E isoforms influence AD pathogenesis, however, remains unclear. Using ES-cell-derived human neurons, we show that Apo. E secreted by glia stimulates neuronal Aβ production with an Apo. E 4 > Apo. E 3 > Apo. E 2 potency rank order. We demonstrate that Apo. E binding to Apo. E receptors activates dual leucine-zipper kinase (DLK), a MAP-kinase that then activates MKK 7 and ERK 1/2 MAP kinases. Activated ERK 1/2 induces c. Fos phosphorylation, stimulating the transcription factor AP-1, which in turn enhances transcription of amyloid-β precursor protein (APP) and thereby increases amyloid-β levels. This molecular mechanism also regulates APP transcription in mice in vivo. Our data describe a novel signal transduction pathway in neurons whereby Apo. E activates a non-canonical MAP kinase cascade that enhances APP transcription and amyloid-β synthesis.