Cognitive Dysfunction in Major Depressive Disorder: Clinical Implications and Interventions |Chapter 6 | Medical Science: Updates and Prospects Vol. 5

 

Cognitive dysfunction is increasingly recognised as a core and disabling component of Major Depressive Disorder (MDD), extending beyond affective symptoms to significantly impairing everyday functioning. While traditional research has largely focused on mood disturbances, growing evidence indicates that deficits in attention, memory, and executive functioning are highly prevalent and often persist even during symptomatic remission. Such impairments contribute substantially to poor psychosocial and occupational outcomes and represent an important determinant of long-term prognosis.

 

This chapter provides a comprehensive narrative review of the patterns and mechanisms of cognitive dysfunction in MDD, integrating findings from recent systematic reviews and meta-analyses. Evidence from the literature indicates that clinically significant cognitive impairment affects approximately half of individuals with MDD, with residual deficits frequently observed following remission of mood symptoms. Among cognitive domains, impairments in executive function, processing speed, and memory demonstrate moderate effect sizes and show strong associations with functional disability and reduced quality of life.

 

The chapter further examines underlying neurobiological and neurophysiological mechanisms, including dysregulation within prefrontal–limbic circuits, hippocampal alterations, hypothalamic–pituitary–adrenal axis hyperactivity, and abnormalities in event-related potentials such as prolonged P300 latency. Clinical implications are discussed, emphasising the importance of routine cognitive assessment and the integration of targeted cognitive interventions alongside standard treatment approaches. Finally, future directions for research and clinical practice are outlined, highlighting the need for individualised cognitive remediation strategies to optimise functional recovery in individuals with MDD.

 

 

Author(s) Details

Sharma S
Department of Physiology, RUHS College of Medical Sciences, Partap Nagar, Jaipur, Rajasthan 302033, India.

 

Kacker S
Department of Physiology, RUHS College of Medical Sciences, Partap Nagar, Jaipur, Rajasthan 302033, India.

 

Saboo N
Department of Physiology, RUHS College of Medical Sciences, Partap Nagar, Jaipur, Rajasthan 302033, India.

 

Please see the book here :- https://doi.org/10.9734/bpi/msup/v5/6939

Pathophysiology and Treatment of Major Depressive Disorder: The Role of Nuclear Receptors Modulate Inflammasomes | Chapter 4 | Medicine and Medical Research: New Perspectives Vol. 7

 

This review summarizes the evidence on nuclear receptors (NRs), such as glucocorticoid receptor, mineralocorticoid receptor, estrogen receptor, aryl hydrocarbon receptor, and peroxisome proliferator-activated receptor, in modulating the inflammasome activity and depression-associated behaviors. Major depressive disorder (MDD) is highly prevalent and is a significant cause of mortality and morbidity worldwide. Currently, conventional pharmacological treatments for MDD produce temporary remission in < 50% of patients; therefore, there is an urgent need for a wider spectrum of novel antidepressants to target newly discovered underlying disease mechanisms. Another important hypothesis of depression, several lines of evidence have established an association between MDD and the neuroimmune pathway, although some psychiatrists have argued about the causal relationship between inflammation and depression. Accumulated evidence has shown that immune inflammation, particularly inflammasome activity, plays an important role in the pathophysiology of MDD. This review provides evidence from an endocrine perspective to understand the role of activated NRs in the pathophysiology of MDD and to provide insight into the discovery of antidepressants with novel mechanisms for this devastating disorder. Cumulative studies have shown that activation of the NRs may directly change the activity of inflammasomes to modulate the levels of mature forms of caspase-1 and IL-1

 

Author (s) Details

Han Wang
The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing 100088, Beijing Province, China.

 

Wei-Jing Kan
The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing 100088, Beijing Province, China.

 

Yuan Feng
The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing 100088, Beijing Province, China.

 

Lei Feng
The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing 100088, Beijing Province, China.

 

Yang Yang
The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing 100088, Beijing Province, China.

 

Pei Chen
The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing 100088, Beijing Province, China.

 

Jing-Jie Xu
The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing 100088, Beijing Province, China.

 

Tian-Mei Si
Department of Clinical Psychopharmacology, Peking University, Institute of Mental Health, Beijing 100191, Beijing Province, China.

Ling Zhang
The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing 100088, Beijing Province, China.

 

Gang Wang
The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing 100088, Beijing Province, China.

 

Jing Du
The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Beijing 100088, Beijing Province, China and State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan University, Kunming 650091, Yunnan Province, China.

 

Please see the book here:- https://doi.org/10.9734/bpi/mmrnp/v7/2092

 

Nano Formulations Targeting the Brain: Advances in Drug Delivery Systems for Cognitive Dysfunction in Depression | Chapter 7 | Novel Aspects on Pharmaceutical Research Vol. 8

The item focuses on various nanotechnological approaches employed to overcome the ancestry-brain obstacle (BBB) and facilitate targeted drug transmittal to the brain, that is the crux in the management of intelligent disorders. Major depressive disorder is a widespread neuropsychiatric condition that frequently goes unnoticed and undiagnosed, specifically in underserved populations lacking approach to healthcare. Studies have demonstrated that the pathophysiology of cavity involves dysfunctions in the dominant glutamatergic structure, impairments in mechanisms managing glutamate clearance and absorption, as well as morphological and maladjusted changes in brain regions guide cognitive-impassioned behaviors. Cognitive dysfunction is a prominent facet of depression, accompanying no new approved drugs for its administration since vortioxetine. Consequently, the development of nanoformulations accompanying enhanced intellect permeability, sustained action, and superior efficiency represents a hopeful future direction. This comprehensive review determines an updated summary of recent progresses in the field of nanomedicines and nano-located drug delivery systems, emphasize their potential for enhancing the efficiency of both novel and existing drugs in the situation of cognitive dysfunction in depression. Additionally, the review climaxes recent studies promoting nano-based formulations for delivering drugs guide the glutamatergic system, such as NMDA receptor modulators, neuroprotective powers, and neurotrophic factors. The potential of nanomedicines in fixing glutamate homeostasis, improving synaptic pliancy, and enhancing neurogenesis is argued. Moreover, the review discusses the advantages of nanocarrier-located strategies in improving drug pharmacokinetics, lowering side effects, and providing maintained drug release profiles, thereby permissive improved healing outcomes and patient compliance.

Author(s) Details:

Jerin James,
Department of Pharmacology, SRM Medical College Hospital and Research Centre, Kattankulathur, Tamilnadu, India.

Jamuna Rani,
Department of Pharmacology, SRM Medical College Hospital and Research Centre, Kattankulathur, Tamilnadu, India.

Sathyanarayanan Varadarajan,
Department of Pharmacology, SRM Medical College Hospital and Research Centre, Kattankulathur, Tamilnadu, India.

Please see the link here: https://stm.bookpi.org/NAPR-V8/article/view/11654

Comparative Efficacy and Safety of Augmentation Therapy with Ziprasidone versus Quetiapine in Patients of Major Depressive Disorder on Escitalopram| Chapter 4 | Current Aspects in Pharmaceutical Research and Development Vol.9

 Many patients with major depressive disorder (MDD) do not respond to traditional antidepressant medication or only respond partially. As a result, augmentation therapy with atypical antipsychotic medications is required in many patients, boosting antidepressant effect and extending partial remission. In patients with MDD, this trial compared augmentation therapy with ziprasidone and quetiapine to escitalopram. A prospective, open-label, randomised, comparative clinical trial was conducted. Part-I of the study comprised adult patients who fulfilled the DSM-5 criteria for MDD and had a HAM-D score of 15 or more on the 17-item version. The critical exclusion criteria were MDD with psychotic symptoms and bipolar illness. After 6 weeks of escitalopram (20 mg per day) treatment, eligible patients who had an inadequate response to treatment (Part-II of the study) were randomly assigned to one of two treatment groups: quetiapine 200 mg once daily or ziprasidone 20 mg twice daily orally for 6 weeks. Efficacy was measured using BDI scores at 2, 4, and 6 weeks during the clinical trial. Adverse drug reactions (ADRs) were minimal in both groups, and none of the research participants required therapy cessation. The addition of quetiapine and ziprasidone to antidepressant therapy was found to be safe and effective in this trial.

Author(s) Details:

Sahil Sharma,
Department of Pharmacology, Pt. BD Sharma PGIMS, Rohtak, Haryana, India.


Jarnail Singh Braich,
Department of Pharmacology, Pt. BD Sharma PGIMS, Rohtak, Haryana, India.

Hitesh Khurana,
State Institute of Mental Health/Department of Psychiatry, Pt. BD Sharma PGIMS, Rohtak, Haryana, India.

Please see the link here: https://stm.bookpi.org/CAPRD-V9/article/view/5964