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Related Concept Videos

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Depressive disorders are a group of mental health conditions characterized by pervasive feelings of sadness, diminished pleasure in life, and a significant impact on daily functioning. These conditions are most prevalent in individuals during their 30s and affect women at twice the rate of men. Contrary to popular belief, younger individuals are generally more susceptible to these disorders than older adults. Two key types of depressive disorders include Major Depressive Disorder (MDD) and...
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Depressive disorders result from a complex interplay of biological, psychological, and sociocultural factors, each contributing uniquely to the development and persistence of the condition. Understanding these factors provides critical insight into the multifaceted nature of depression.
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Depression is a prevalent mental illness marked by persistent sadness and lack of interest in previously enjoyable activities. It can take several forms, including major depression, persistent depressive disorder, and bipolar I and II disorders. Symptoms range from emotional changes like chronic worry to physical changes like sleep disturbances and suicidal thoughts. From a neurobiological perspective, depression is believed to be triggered by abnormalities in the brain's prefrontal cortex,...
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Anorexia nervosa is a complex and severe eating disorder characterized by an intense fear of weight gain, an unrelenting pursuit of thinness, and a distorted body image. It often leads to dangerously low body weight relative to an individual's age and height. This disorder is marked by significant physical and psychological consequences, making it one of the most life-threatening psychiatric illnesses.
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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Atypical antidepressants, including bupropion (Wellbutrin), mirtazapine (Remeron), nefazodone (Serzone), trazodone (Desyrel), and vilazodone (Viibryd), offer unique mechanisms of action. Bupropion weakly inhibits dopamine and norepinephrine reuptake, aiding depression treatment and smoking cessation, with a low risk of sexual dysfunction. Mirtazapine enhances serotonin and norepinephrine neurotransmission, leading to sedation, increased appetite, and weight gain. As a result, it helps treat...
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The Unpredictable Chronic Mild Stress Protocol for Inducing Anhedonia in Mice
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Anhedonia and Depressive Disorders.

Alessandro Serretti1

  • 1Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.

Clinical Psychopharmacology and Neuroscience : the Official Scientific Journal of the Korean College of Neuropsychopharmacology
|July 10, 2023
PubMed
Summary
This summary is machine-generated.

Anhedonia, a core symptom of depression, involves reward processing deficits and is a risk factor for suicidality. Targeted treatments beyond traditional antidepressants are needed for this condition, which is often independent of depression severity.

Keywords:
AnhedoniaAntidepressantsMajor depressive disorderPsychopharmacology

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Genetics

Background:

  • Anhedonia is a key symptom in depression and other psychiatric disorders.
  • It encompasses a range of reward processing deficits, gaining significant research attention.
  • Anhedonia is a risk factor for suicidal behaviors, potentially independent of episode severity.

Purpose of the Study:

  • To review the multifaceted nature of anhedonia.
  • To explore its neurobiological underpinnings and genetic components.
  • To assess current and emerging treatment strategies.

Main Methods:

  • Literature review of anhedonia research.
  • Analysis of neurophysiological and genetic studies.
  • Evaluation of treatment efficacy for anhedonia.

Main Results:

  • Anhedonia is linked to inflammation and alterations in striatal and prefrontal areas, involving dopamine.
  • Genetic factors contribute to anhedonia, with polygenic risk scores showing predictive potential.
  • Selective serotonin reuptake inhibitors have limited efficacy, and some may worsen anhedonia.

Conclusions:

  • Anhedonia requires specific assessment and targeted interventions.
  • Treatments like agomelatine, vortioxetine, ketamine, TMS, and psychotherapy show promise.
  • Anhedonia is at least partially independent of depression, necessitating distinct treatment approaches.