서울特別市 銅雀區 舍堂洞입자 물리학의 입자기본 입자페르미온쿼크위(u)아래(d)맵시(c)기묘(s)꼭대기(t)바닥(b)렙톤전자(e−)/양전자(e+)뮤온(μ−/μ+)타우 입자(τ−/τ+)중성미자 전자 중성미자/전자 반중성미자뮤온 중성미자/뮤온 반중성미자타우 중성미자/타우 반중성미자보손게이지 보손 (광자W · Z보손글루온)스칼라 보손(힉스 보손)미관측 입자대통일 이론 등액시온(A0)마요론(J)X · Y보손W' · Z' 보손비활성 중성미자자기 홀극테크니컬러 관련 입자초대칭짝게이지노글루이노중력미자 (골드스티노)뉴트랄리노 (포티노힉시노지노)차지노 (위노힉시노)색시온액시노스페르미온스쿼크 (스칼라 위 쿼크, 스칼라 아래 쿼크, 스칼라 맵시 쿼크, 스칼라 기묘 쿼크, 스칼라 꼭대기 쿼크, 스칼라 바닥 쿼크)슬렙톤 (스엘렉트론, 스뮤온, 스타우온, 스뉴트리노, 스뮤온 스뉴트리노, 스타우 스뉴트리노)양자 중력 및 끈 이론중력자딜라톤라디온(중력스칼라)중력광자기타유령 입자골드스톤 보손타키온순간자합성 입자강입자중입자핵자(N) (양성자(p)중성자(n))Δ(델타)Λ(람다)Σ(시그마)Ξ(크시)Ω(오메가)맛깔없는 가벼운 중간자π(파이온)ρ(로)η(에타)·η′(에타 프라임)φ(피)ω(오메가)a(에이)b(비)f(에프)·f′(에프 프라임)h(에이치)·h′(에이치 프라임)맛깔없는 무거운 중간자J/ψ(제이/프시)ϒ(입실론)θ(세타)χ(키)ηc/b/t(에타 쿼코늄)hc/b/t맛깔있는 중간자K(케이온)DBT기타원자핵원자분자별난 원자 오늄포지트로늄뮤오늄 등펜타쿼크미관측 입자테트라쿼크글루볼중간자 분자준입자솔리톤엑시톤마그논포논플라스몬폴라리톤폴라론로톤목록기타 가설 입자무의식초자아트라우마방어기제정신분석게슈탈트 붕괴고전적 조건형성조작적 조건형성인지부조화바넘 효과심리 검사성격 검사초두효과설단 현상칵테일 파티 효과전경-배경 이론깨진 유리창 이론정보처리이론루시퍼 이펙트스탠퍼드 감옥 실험편안한 복제인간 증후군원인론목적론해석 수준 이론심리치료인문학재난심리학(disaster psychology)군사심리학(영어판)군중심리학자살 예방환경심리학깨진 유리창 이론범죄예방 환경설계심리역사학(영어판)로이드 드마우스(영어판)의상심리학(clothing psychology)의사소통(휴먼 커뮤니케이션)대인간 커뮤니케이션(영어판)잔소리 (심리)(영어판)편집성 인격 장애폭력 / 가정폭력아동학대 / 동물학대힐가드와 애트킨슨의 심리학 원론(Atkinson & Hilgard's Introduction to Psychology)볼더 모델찰스 다윈심리학역사심리학자연구 분야감정생물심리학임상심리학인지심리학인지 신경과학비교심리학비판심리학문화심리학발달심리학진화심리학실험심리학개인심리학해방심리학수리심리학매체심리학약물심리학신경심리학수행심리학성격심리학생리심리학정치심리학긍정심리학심리언어학정신병리학정신물리학심리생리학정성적 심리 연구정량적 심리 연구사회심리학이론심리학교육심리학군중심리학스포츠심리학프시응용 분야심리 실험임상심리학상담심리학교육심리학법정심리학건강심리학산업 및 조직 심리학법심리학산업 건강심리학관계심리학학교심리학스포츠심리학음향심리학체제심리학심리철학시각심리학접근 방법분석심리학행동주의인지주의인지 행동 치료기술심리학실존주의 상담가족 치료인지 정서 행동 치료여성주의 상담게슈탈트 치료인본주의심리학초심리학이야기 치료정신분석학정신 역동 치료초개인심리학주요 심리학자버러스 프레더릭 스키너장 피아제지그문트 프로이트오토 랑크멜라니 클라인앨버트 반두라레온 페스팅거로이 샤퍼칼 로저스스탠리 샤흐터닐 엘가 밀러에드워드 손다이크에이브러햄 매슬로고던 올포트에릭 에릭슨한스 아이젠크윌프레드 비용윌리엄 제임스데이비드 맥클랜드앨버트 엘리스아론 벡레이몬드 캐텔존 B. 왓슨쿠르트 르빈도널드 올딩 헤브조지 밀러클라크 헐제롬 케이건카를 융이반 파블로프앙드레 그린알프레트 아들러사회과학주류경제학 거시경제학미시경제학계량경제학수리경제학법학 공법학사법학법계학법제사학판례학사학 경제사학군사사학문화사학사회사학세계사학정치사학역사보조학사회학 농촌사회학도시사회학범죄학인구통계학인터넷사회학언어학 기호학인류학 고고학문화인류학사회인류학체질인류학정치학 국제관계학비교정치학정치철학공공정책학지리학 기술지리학인문지리학자연지리학환경지리학응용개발학경영학군 경영학행정학계획학군 토지이용계획연구지역계획연구도시계획연구공중보건학과학기술학과학철학군 경제철학사회과학철학심리철학역사철학교육학기술사학과학학군 과학사학양자과학학사회복지학상업학언론정보학역사사회학인간동물학인지과학인류생태학정보과학정치경제학정치사회학정치생태학젠더학지역과학지역학환경학군 환경사회과학환경연구문화연구미디어연구세계화연구식품연구지역연구채식연구해부학뼈대뼈몸통뼈대 머리뼈척추가슴우리팔다리뼈대 팔뼈대다리뼈대골수연골유리연골섬유연골탄력연골관절섬유관절연골관절윤활관절근육계골격근민무늬근심장근내분비계뇌하수체시상하부솔방울샘갑상샘부갑상샘가슴샘부신이자정소난소순환계심혈관계심장혈관 동맥정맥모세혈관대동맥대정맥폐동맥폐정맥혈액 혈장적혈구백혈구혈소판림프계림프관림프절비장가슴샘편도파이어판점막관련림프조직비뇨계콩팥요관방광요도생식계남성고환부고환정관정삭요도정낭전립샘망울요도샘음낭음경귀두포피여성난소자궁관자궁질질입구주름음문대음순소음순젖샘소화계소화관입인두식도위작은창자 샘창자공장회장큰창자 맹장결장곧은창자항문소화샘침샘이자쓸개간신경계중추신경계 뇌척수말초신경계 몸신경계자율신경계 교감신경계부교감신경계눈귀코혀피부계피부모낭땀샘피지샘손발톱유방호흡계비강인두후두기관기관지허파외분비계땀샘망울요도샘스킨샘젖샘전립샘전미골부샘점액정낭침샘코딱지큰질어귀샘생물학의 주요 분야생물학의 분야계생명학고생물학고유전학균학기생충학동물학면역학미생물학발생생물학 (발생학)병리학보전생물학분류학분자생물학분자세포유전학생리학생물리학생물정보학생물통계학생태학생화학세포생물학세포유전학수리생물학시간생물학식물학신경과학약리학역학우주생물학유전체학유전학위생학인간생물학조직학진화생물학해부학해양생물학생물학의 가설들자연발생설Personality disorder classificationGeneral classificationsDimensionalCategoricalMulti-axialPrototypalRelationalStructuralICD classifications (ICD-10)SchizotypalSchizotypalSpecificAnankastic personality disorderAnxious (avoidant)DependentDissocialEmotionallyunstableHistrionicParanoidSchizoidOtherEccentricHaltloseImmatureNarcissisticPassive–aggressivePsychoneuroticOrganicOrganicUnspecifiedUnspecifiedDSM classificationsDSM-III-R onlySadisticSelf-defeating (masochistic)DSM-IV onlyPersonality disorder not otherwise specifiedAppendix B (proposed)DepressiveNegativistic (passive–aggressive)DSM-5Cluster A (odd)ParanoidSchizoidSchizotypalCluster B (dramatic)AntisocialBorderlineHistrionicNarcissisticCluster C (anxious)AvoidantDependentObsessive-compulsiveOtherOther specifiedUnspecifiedAlternative DSM-5 Modelfor Personality DisordersSpecificAntisocialAvoidantBorderlineNarcissisticObsessive-compulsiveSchizotypalGeneralTrait SpecifiedvteMental disorders (Classification)Adult personality and behaviorChildhood and learningMood (affective)Neurological and symptomaticNeurotic, stress-related and somatoformPhysiological and physical behaviorPsychoactive substances, substance abuse and substance-relatedSchizophrenia, schizotypal and delusionalSymptoms and uncategorized시시비비 是是非非right and[or] wrong불문곡직without inquiring into the right or wrong

 서울特別市 銅雀區 舍堂洞입자 물리학의 입자기본 입자페르미온쿼크위(u)아래(d)맵시(c)기묘(s)꼭대기(t)바닥(b)렙톤전자(e−)/양전자(e+)뮤온(μ−/μ+)타우 입자(τ−/τ+)중성미자 전자 중성미자/전자 반중성미자뮤온 중성미자/뮤온 반중성미자타우 중성미자/타우 반중성미자보손게이지 보손 (광자W · Z보손글루온)스칼라 보손(힉스 보손)미관측 입자대통일 이론 등액시온(A0)마요론(J)X · Y보손W' · Z' 보손비활성 중성미자자기 홀극테크니컬러 관련 입자초대칭짝게이지노글루이노중력미자 (골드스티노)뉴트랄리노 (포티노힉시노지노)차지노 (위노힉시노)색시온액시노스페르미온스쿼크 (스칼라 위 쿼크, 스칼라 아래 쿼크, 스칼라 맵시 쿼크, 스칼라 기묘 쿼크, 스칼라 꼭대기 쿼크, 스칼라 바닥 쿼크)슬렙톤 (스엘렉트론, 스뮤온, 스타우온, 스뉴트리노, 스뮤온 스뉴트리노, 스타우 스뉴트리노)양자 중력 및 끈 이론중력자딜라톤라디온(중력스칼라)중력광자기타유령 입자골드스톤 보손타키온순간자합성 입자강입자중입자핵자(N) (양성자(p)중성자(n))Δ(델타)Λ(람다)Σ(시그마)Ξ(크시)Ω(오메가)맛깔없는 가벼운 중간자π(파이온)ρ(로)η(에타)·η′(에타 프라임)φ(피)ω(오메가)a(에이)b(비)f(에프)·f′(에프 프라임)h(에이치)·h′(에이치 프라임)맛깔없는 무거운 중간자J/ψ(제이/프시)ϒ(입실론)θ(세타)χ(키)ηc/b/t(에타 쿼코늄)hc/b/t맛깔있는 중간자K(케이온)DBT기타원자핵원자분자별난 원자 오늄포지트로늄뮤오늄 등펜타쿼크미관측 입자테트라쿼크글루볼중간자 분자준입자솔리톤엑시톤마그논포논플라스몬폴라리톤폴라론로톤목록기타 가설 입자무의식초자아트라우마방어기제정신분석게슈탈트 붕괴고전적 조건형성조작적 조건형성인지부조화바넘 효과심리 검사성격 검사초두효과설단 현상칵테일 파티 효과전경-배경 이론깨진 유리창 이론정보처리이론루시퍼 이펙트스탠퍼드 감옥 실험편안한 복제인간 증후군원인론목적론해석 수준 이론심리치료인문학재난심리학(disaster psychology)군사심리학(영어판)군중심리학자살 예방환경심리학깨진 유리창 이론범죄예방 환경설계심리역사학(영어판)로이드 드마우스(영어판)의상심리학(clothing psychology)의사소통(휴먼 커뮤니케이션)대인간 커뮤니케이션(영어판)잔소리 (심리)(영어판)편집성 인격 장애폭력 / 가정폭력아동학대 / 동물학대힐가드와 애트킨슨의 심리학 원론(Atkinson & Hilgard's Introduction to Psychology)볼더 모델찰스 다윈심리학역사심리학자연구 분야감정생물심리학임상심리학인지심리학인지 신경과학비교심리학비판심리학문화심리학발달심리학진화심리학실험심리학개인심리학해방심리학수리심리학매체심리학약물심리학신경심리학수행심리학성격심리학생리심리학정치심리학긍정심리학심리언어학정신병리학정신물리학심리생리학정성적 심리 연구정량적 심리 연구사회심리학이론심리학교육심리학군중심리학스포츠심리학프시응용 분야심리 실험임상심리학상담심리학교육심리학법정심리학건강심리학산업 및 조직 심리학법심리학산업 건강심리학관계심리학학교심리학스포츠심리학음향심리학체제심리학심리철학시각심리학접근 방법분석심리학행동주의인지주의인지 행동 치료기술심리학실존주의 상담가족 치료인지 정서 행동 치료여성주의 상담게슈탈트 치료인본주의심리학초심리학이야기 치료정신분석학정신 역동 치료초개인심리학주요 심리학자버러스 프레더릭 스키너장 피아제지그문트 프로이트오토 랑크멜라니 클라인앨버트 반두라레온 페스팅거로이 샤퍼칼 로저스스탠리 샤흐터닐 엘가 밀러에드워드 손다이크에이브러햄 매슬로고던 올포트에릭 에릭슨한스 아이젠크윌프레드 비용윌리엄 제임스데이비드 맥클랜드앨버트 엘리스아론 벡레이몬드 캐텔존 B. 왓슨쿠르트 르빈도널드 올딩 헤브조지 밀러클라크 헐제롬 케이건카를 융이반 파블로프앙드레 그린알프레트 아들러사회과학주류경제학 거시경제학미시경제학계량경제학수리경제학법학 공법학사법학법계학법제사학판례학사학 경제사학군사사학문화사학사회사학세계사학정치사학역사보조학사회학 농촌사회학도시사회학범죄학인구통계학인터넷사회학언어학 기호학인류학 고고학문화인류학사회인류학체질인류학정치학 국제관계학비교정치학정치철학공공정책학지리학 기술지리학인문지리학자연지리학환경지리학응용개발학경영학군 경영학행정학계획학군 토지이용계획연구지역계획연구도시계획연구공중보건학과학기술학과학철학군 경제철학사회과학철학심리철학역사철학교육학기술사학과학학군 과학사학양자과학학사회복지학상업학언론정보학역사사회학인간동물학인지과학인류생태학정보과학정치경제학정치사회학정치생태학젠더학지역과학지역학환경학군 환경사회과학환경연구문화연구미디어연구세계화연구식품연구지역연구채식연구해부학뼈대뼈몸통뼈대 머리뼈척추가슴우리팔다리뼈대 팔뼈대다리뼈대골수연골유리연골섬유연골탄력연골관절섬유관절연골관절윤활관절근육계골격근민무늬근심장근내분비계뇌하수체시상하부솔방울샘갑상샘부갑상샘가슴샘부신이자정소난소순환계심혈관계심장혈관 동맥정맥모세혈관대동맥대정맥폐동맥폐정맥혈액 혈장적혈구백혈구혈소판림프계림프관림프절비장가슴샘편도파이어판점막관련림프조직비뇨계콩팥요관방광요도생식계남성고환부고환정관정삭요도정낭전립샘망울요도샘음낭음경귀두포피여성난소자궁관자궁질질입구주름음문대음순소음순젖샘소화계소화관입인두식도위작은창자 샘창자공장회장큰창자 맹장결장곧은창자항문소화샘침샘이자쓸개간신경계중추신경계 뇌척수말초신경계 몸신경계자율신경계 교감신경계부교감신경계눈귀코혀피부계피부모낭땀샘피지샘손발톱유방호흡계비강인두후두기관기관지허파외분비계땀샘망울요도샘스킨샘젖샘전립샘전미골부샘점액정낭침샘코딱지큰질어귀샘생물학의 주요 분야생물학의 분야계생명학고생물학고유전학균학기생충학동물학면역학미생물학발생생물학 (발생학)병리학보전생물학분류학분자생물학분자세포유전학생리학생물리학생물정보학생물통계학생태학생화학세포생물학세포유전학수리생물학시간생물학식물학신경과학약리학역학우주생물학유전체학유전학위생학인간생물학조직학진화생물학해부학해양생물학생물학의 가설들자연발생설Personality disorder classificationGeneral classificationsDimensionalCategoricalMulti-axialPrototypalRelationalStructuralICD classifications (ICD-10)SchizotypalSchizotypalSpecificAnankastic personality disorderAnxious (avoidant)DependentDissocialEmotionallyunstableHistrionicParanoidSchizoidOtherEccentricHaltloseImmatureNarcissisticPassive–aggressivePsychoneuroticOrganicOrganicUnspecifiedUnspecifiedDSM classificationsDSM-III-R onlySadisticSelf-defeating (masochistic)DSM-IV onlyPersonality disorder not otherwise specifiedAppendix B (proposed)DepressiveNegativistic (passive–aggressive)DSM-5Cluster A (odd)ParanoidSchizoidSchizotypalCluster B (dramatic)AntisocialBorderlineHistrionicNarcissisticCluster C (anxious)AvoidantDependentObsessive-compulsiveOtherOther specifiedUnspecifiedAlternative DSM-5 Modelfor Personality DisordersSpecificAntisocialAvoidantBorderlineNarcissisticObsessive-compulsiveSchizotypalGeneralTrait SpecifiedvteMental disorders (Classification)Adult personality and behaviorChildhood and learningMood (affective)Neurological and symptomaticNeurotic, stress-related and somatoformPhysiological and physical behaviorPsychoactive substances, substance abuse and substance-relatedSchizophrenia, schizotypal and delusionalSymptoms and uncategorized시시비비 是是非非right and[or] wrong불문곡직without inquiring into the right or wrong










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Major depressive disorder (MDD), also known as clinical depression, is a mental disorder[10] characterized by at least two weeks of pervasive low mood, low self-esteem, and loss of interest or pleasure in normally enjoyable activities. Introduced by a group of US clinicians in the mid-1970s,[11] the term was adopted by the American Psychiatric Association for this symptom cluster under mood disorders in the 1980 version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), and has become widely used since. The disorder causes the second-most years lived with disability, after lower back pain.[12] The diagnosis of major depressive disorder is based on the person's reported experiences, behavior reported by family or friends, and a mental status examination.[13] There is no laboratory test for the disorder, but testing may be done to rule out physical conditions that can cause similar symptoms.[13] The most common time of onset is in a person's 20s,[3][4] with females affected about three times as often as males.[14] The course of the disorder varies widely, from one episode lasting months to a lifelong disorder with recurrent major depressive episodes. Those with major depressive disorder are typically treated with psychotherapy and antidepressant medication.[1] While a mainstay of treatment, the clinical efficacy of antidepressants is controversial.[15][16][17][18] Hospitalization (which may be involuntary) may be necessary in cases with associated self-neglect or a significant risk of harm to self or others. Electroconvulsive therapy (ECT) may be considered if other measures are not effective.[1] Major depressive disorder is believed to be caused by a combination of genetic, environmental, and psychological factors,[1] with about 40% of the risk being genetic.[5] Risk factors include a family history of the condition, major life changes, childhood traumas, environmental lead exposure,[19] certain medications, chronic health problems, and substance use disorders.[1][5] It can negatively affect a person's personal life, work life, or education, and cause issues with a person's sleeping habits, eating habits, and general health.[1][5] Signs and symptoms See also: Digital media use and mental health § Depression An 1892 lithograph of a woman diagnosed with melancholia A person having a major depressive episode usually exhibits a low mood, which pervades all aspects of life, and an inability to experience pleasure in previously enjoyable activities.[20] Depressed people may be preoccupied with or ruminate over thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness or hopelessness.[21] Other symptoms of depression include poor concentration and memory,[22] withdrawal from social situations and activities, reduced sex drive, irritability, and thoughts of death or suicide. Insomnia is common; in the typical pattern, a person wakes very early and cannot get back to sleep. Hypersomnia, or oversleeping, can also happen,[23] as well as day-night rhythm disturbances, such as diurnal mood variation.[24] Some antidepressants may also cause insomnia due to their stimulating effect.[25] In severe cases, depressed people may have psychotic symptoms. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant.[26] People who have had previous episodes with psychotic symptoms are more likely to have them with future episodes.[27] A depressed person may report multiple physical symptoms such as fatigue, headaches, or digestive problems; physical complaints are the most common presenting problem in developing countries, according to the World Health Organization's criteria for depression.[28] Appetite often decreases, resulting in weight loss, although increased appetite and weight gain occasionally occur.[29] Major depression significantly affects a person's family and personal relationships, work or school life, sleeping and eating habits, and general health.[30] Family and friends may notice agitation or lethargy.[23] Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness,[31] and a more noticeable slowing of movements.[32] Depressed children may often display an irritable rather than a depressed mood;[23] most lose interest in school and show a steep decline in academic performance.[33] Diagnosis may be delayed or missed when symptoms are interpreted as "normal moodiness".[34] Elderly people may not present with classical depressive symptoms.[35] Diagnosis and treatment is further complicated in that the elderly are often simultaneously treated with a number of other drugs, and often have other concurrent diseases.[35] Cause Further information: Biology of depression and Epigenetics of depression A cup analogy demonstrating the diathesis–stress model that under the same amount of stressors, person 2 is more vulnerable than person 1, because of their predisposition[36] The etiology of depression is not yet fully understood.[37][38][39] The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression.[5][40] The diathesis–stress model specifies that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic,[41][42] implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.[43] American psychiatrist Aaron Beck suggested that a triad of automatic and spontaneous negative thoughts about the self, the world or environment, and the future may lead to other depressive signs and symptoms.[44][45] Genetics Genes play a major role in the development of depression.[46] Family and twin studies suggest that genetic factors account for nearly 40% of the variation in risk for major depressive disorder. Like most psychiatric disorders, major depression is likely shaped by a combination of many individual genetic influences.[47] In 2018, a genome-wide association study discovered 44 genetic variants linked to risk for major depression;[48] a 2019 study found 102 variants in the genome linked to depression.[49] However, it appears that major depression is less heritable compared to bipolar disorder and schizophrenia.[50][51] Research focusing on specific candidate genes has been criticized for its tendency to generate false positive findings.[52] There are also other efforts to examine interactions between life stress and polygenic risk for depression.[53] Other health problems Depression can also arise after a chronic or terminal medical condition, such as HIV/AIDS or asthma, and may be labeled "secondary depression".[54][55] It is unknown whether the underlying diseases induce depression through effect on quality of life, or through shared etiologies (such as degeneration of the basal ganglia in Parkinson's disease or immune dysregulation in asthma).[56] Depression may also be iatrogenic (the result of healthcare), such as drug-induced depression. Therapies associated with depression include interferons, beta blockers,[57] isotretinoin,[58] contraceptives,[57] cardiac agents,[59] anticonvulsants,[60] and hormonal agents.[61] Celiac disease is another possible contributing factor.[62] Substance use in early age is associated with increased risk of developing depression later in life.[63] Depression occurring after giving birth is called postpartum depression and is thought to be the result of hormonal changes associated with pregnancy.[64] Seasonal affective disorder, a type of depression associated with seasonal changes in sunlight, is thought to be triggered by decreased sunlight.[65] Vitamin B2, B6 and B12 deficiency may cause depression in females.[66] A 2025 study found that, among more than 172,500 adults in the UK aged 39 and older, those with a history of depression experienced the onset of chronic illnesses approximately 30% earlier than those without depression.[67] Environmental Adverse childhood experiences (incorporating childhood abuse, neglect and family dysfunction) markedly increase the risk of major depression, especially if more than one type.[68] Childhood trauma also correlates with severity of depression, poor responsiveness to treatment and length of illness.[69] Some are more susceptible than others to developing mental illness such as depression after trauma, and various genes have been suggested to control susceptibility.[70] Couples in unhappy marriages have a higher risk of developing clinical depression.[71] There appears to be a link between air pollution and depression and suicide. There may be an association between long-term PM2.5 exposure and depression, and a possible association between short-term PM10 exposure and suicide.[72] Living alone has been found to increase the risk of depression by 42%.[6] Pathophysiology Further information: Biology of depression and Epigenetics of depression The pathophysiology of depression is not completely understood, but current theories center around monoaminergic systems, the circadian rhythm, immunological dysfunction, HPA-axis dysfunction, and structural or functional abnormalities of emotional circuits. Derived from the effectiveness of monoaminergic drugs in treating depression, the monoamine theory posits that insufficient activity of monoamine neurotransmitters is the primary cause of depression. Evidence for the monoamine theory comes from multiple areas. First, acute depletion of tryptophan—a necessary precursor of serotonin and a monoamine—can cause depression in those in remission or relatives of people who are depressed, suggesting that decreased serotonergic neurotransmission is important in depression.[73] Second, the correlation between depression risk and polymorphisms in the 5-HTTLPR gene, which codes for serotonin receptors, suggests a link.[74] Third, decreased size of the locus coeruleus, reduced activity of tyrosine hydroxylase, increased density of alpha-2 adrenergic receptor, and evidence from rat models suggest decreased adrenergic neurotransmission in depression.[75] Furthermore, decreased levels of homovanillic acid, altered response to dextroamphetamine, responses of depressive symptoms to dopamine receptor agonists, decreased dopamine receptor D1 binding in the striatum,[76] and polymorphism of dopamine receptor genes implicate dopamine, another monoamine, in depression.[77][78] Lastly, increased activity of monoamine oxidase, which degrades monoamines, has been associated with depression.[79] However, the monoamine theory is inconsistent with observations that serotonin depletion does not cause depression in healthy persons, that antidepressants instantly increase levels of monoamines but take weeks to work, and the existence of atypical antidepressants which can be effective despite not targeting this pathway.[80] One proposed explanation for the therapeutic lag, and further support for the deficiency of monoamines, is a desensitization of self-inhibition in raphe nuclei by the increased serotonin mediated by antidepressants.[81] However, disinhibition of the dorsal raphe has been proposed to occur as a result of decreased serotonergic activity in tryptophan depletion, resulting in a depressed state mediated by increased serotonin. Further countering the monoamine hypothesis is the fact that rats with lesions of the dorsal raphe are not more depressive than controls; the finding of increased jugular 5-HIAA in people who are depressed that normalized with selective serotonin reuptake inhibitor (SSRI) treatment, and the preference for carbohydrates in people who are depressed.[82] Already limited, the monoamine hypothesis has been further oversimplified when presented to the general public.[83] A 2022 review found no consistent evidence supporting the serotonin hypothesis linking serotonin levels and depression.[84] HPA-axis abnormalities have been suggested in depression given the association of CRHR1 with depression and the increased frequency of dexamethasone test non-suppression in people who are depressed. However, this abnormality is not adequate as a diagnosis tool because its sensitivity is only 44%.[85] These stress-related abnormalities are thought to be the cause of hippocampal volume reductions seen in people who are depressed.[86] Furthermore, a meta-analysis yielded decreased dexamethasone suppression, and increased response to psychological stressors.[87] Further abnormal results have been obscured with the cortisol awakening response, with increased response being associated with depression.[88] There is also a connection between the gut microbiome and the central nervous system, otherwise known as the Gut-Brain axis, which is a two-way communication system between the brain and the gut. Experiments have shown that microbiota in the gut can play an important role in depression, as people with MDD often have gut-brain dysfunction. One analysis showed that those with MDD have different bacteria in their guts. Bacteria Bacteroidetes and Firmicutes were most affected in people with MDD, and they are also impacted in people with irritable bowel syndrome.[89] Another study showed that people with IBS have a higher chance of developing depression, which shows the two are connected.[90] There is even evidence suggesting that altering the microbes in the gut can have regulatory effects on developing depression.[89] Theories unifying neuroimaging findings have been proposed. The first model proposed is the limbic-cortical model, which involves hyperactivity of the ventral paralimbic regions and hypoactivity of frontal regulatory regions in emotional processing.[91] Another model, the cortico-striatal model, suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures result in depression.[92] Another model proposes hyperactivity of salience structures in identifying negative stimuli and hypoactivity of cortical regulatory structures resulting in a negative emotional bias and depression, consistent with emotional bias studies.[93] Immune pathogenesis theories on depression The newer field of psychoneuroimmunology, the study between the immune system and the nervous system and emotional state, suggests that cytokines may impact depression. Immune system abnormalities have been observed, including increased levels of cytokines -cells produced by immune cells that affect inflammation- involved in generating sickness behavior, creating a pro-inflammatory profile in MDD.[94][95][96] Some people with depression have increased levels of pro-inflammatory cytokines and some have decreased levels of anti-inflammatory cytokines.[97] Research suggests that treatments can reduce pro-inflammatory cell production, like the experimental treatment of ketamine with treatment-resistant depression.[98] With this, in MDD, people will more likely have a Th-1 dominant immune profile, which is a pro-inflammatory profile. This suggests that there are components of the immune system affecting the pathology of MDD.[99] Another way cytokines can affect depression is in the kynurenine pathway, and when this is overactivated, it can cause depression. This can be due to too much microglial activation and too little astrocytic activity. When microglia get activated, they release pro-inflammatory cytokines that cause an increase in the production of COX2. This, in turn, causes the production of PGE2, which is a prostaglandin, and this catalyzes the production of indolamine, IDO. IDO causes tryptophan to get converted into kynurenine, and kynurenine becomes quinolinic acid.[100] Quinolinic acid is an agonist for NMDA receptors, so it activates the pathway. Studies have shown that the post-mortem brains of patients with MDD have higher levels of quinolinic acid than people who did not have MDD. With this, researchers have also seen that the concentration of quinolinic acid correlates to the severity of depressive symptoms.[101] Diagnosis Assessment Further information: Rating scales for depression Caricature of a man with depression A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist,[30] who records the person's current circumstances, biographical history, current symptoms, family history, and alcohol and drug use. The assessment also includes a mental state examination, which is an assessment of the person's current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harm or suicide, and an absence of positive thoughts or plans.[30] Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-care clinicians.[102] This issue is even more marked in developing countries.[103] Rating scales are not used to diagnose depression, but they provide an indication of the severity of symptoms for a time period, so a person who scores above a given cut-off point can be more thoroughly evaluated for a depressive disorder diagnosis. Several rating scales are used for this purpose;[104] these include the Hamilton Rating Scale for Depression,[105] the Beck Depression Inventory[106] or the Suicide Behaviors Questionnaire-Revised.[107] Primary-care physicians have more difficulty with underrecognition and undertreatment of depression compared to psychiatrists. These cases may be missed because for some people with depression, physical symptoms often accompany depression. In addition, there may also be barriers related to the person, provider, and/or the medical system. Non-psychiatrist physicians have been shown to miss about two-thirds of cases, although there is some evidence of improvement in th

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  Major depressive disorder   ( MDD ), also known as   clinical depression , is a   mental disorder [ 10 ]   characterized by at least two weeks of pervasive   low mood , low   self-esteem , and   loss of interest or pleasure   in normally enjoyable activities. Introduced by a group of US clinicians in the mid-1970s, [ 11 ]   the term was adopted by the   American Psychiatric Association   for this   symptom cluster   under   mood disorders   in the 1980 version of the   Diagnostic and Statistical Manual of Mental Disorders   (DSM-III), and has become widely used since. The disorder causes the second-most   years lived with disability , after   lower back pain . [ 12 ] The diagnosis of major depressive disorder is based on the person's reported experiences, behavior reported by family or friends, and a  mental status examination . [ 13 ]  There is no laboratory test for the diso...
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Psychology is the scientific study of the mind and behavior.[1][2] Its subject matter includes the behavior of humans and nonhumans, both conscious and unconscious phenomena, and mental processes such as thoughts, feelings, and motives. Psychology is an academic discipline of immense scope, crossing the boundaries between the natural and social sciences. Biological psychologists seek an understanding of the emergent properties of brains, linking the discipline to neuroscience. As social scientists, psychologists aim to understand the behavior of individuals and groups.[3][4] A professional practitioner or researcher involved in the discipline is called a psychologist. Some psychologists can also be classified as behavioral or cognitive scientists. Some psychologists attempt to understand the role of mental functions in individual and social behavior. Others explore the physiological and neurobiological processes that underlie cognitive functions and behaviors. As part of an interdisciplinary field, psychologists are involved in research on perception, cognition, attention, emotion, intelligence, subjective experiences, motivation, brain functioning, and personality. Psychologists' interests extend to interpersonal relationships, psychological resilience, family resilience, and other areas within social psychology. They also consider the unconscious mind.[5] Research psychologists employ empirical methods to infer causal and correlational relationships between psychosocial variables. Some, but not all, clinical and counseling psychologists rely on symbolic interpretation. While psychological knowledge is often applied to the assessment and treatment of mental health problems, it is also directed towards understanding and solving problems in several spheres of human activity. By many accounts, psychology ultimately aims to benefit society.[6][7][8] Many psychologists are involved in some kind of therapeutic role, practicing psychotherapy in clinical, counseling, or school settings. Other psychologists conduct scientific research on a wide range of topics related to mental processes and behavior. Typically the latter group of psychologists work in academic settings (e.g., universities, medical schools, or hospitals). Another group of psychologists is employed in industrial and organizational settings.[9] Yet others are involved in work on human development, aging, sports, health, forensic science, education, and the media.

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 Psychology is the scientific study of the mind and behavior.[1][2] Its subject matter includes the behavior of humans and nonhumans, both conscious and unconscious phenomena, and mental processes such as thoughts, feelings, and motives. Psychology is an academic discipline of immense scope, crossing the boundaries between the natural and social sciences. Biological psychologists seek an understanding of the emergent properties of brains, linking the discipline to neuroscience. As social scientists, psychologists aim to understand the behavior of individuals and groups.[3][4] A professional practitioner or researcher involved in the discipline is called a psychologist. Some psychologists can also be classified as behavioral or cognitive scientists. Some psychologists attempt to understand the role of mental functions in individual and social behavior. Others explore the physiological and neurobiological processes that underlie cognitive functions and behaviors. As part of an interd...
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