Assessing the efficacy and safety of combined buspirone and venlafaxine treatment in late-life depression accompanied by cognitive impairment: A randomized controlled trial DOI

ShuJia Hu,

Ke Chen,

Qiuxia Xu

et al.

General Hospital Psychiatry, Journal Year: 2024, Volume and Issue: 91, P. 1 - 10

Published: Sept. 3, 2024

Language: Английский

Microstructural brain abnormalities, fatigue, and cognitive dysfunction after mild COVID-19 DOI Creative Commons

Lucas Scardua-Silva,

Beatriz Amorim Da Costa, Ítalo Karmann Aventurato

et al.

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: Jan. 19, 2024

Abstract Although some studies have shown neuroimaging and neuropsychological alterations in post-COVID-19 patients, fewer combined neuropsychology evaluations of individuals who presented a mild acute infection. Here we investigated cognitive dysfunction brain changes group mildly infected individuals. We conducted cross-sectional study 97 consecutive subjects (median age 41 years) without current or history psychiatric symptoms (including anxiety depression) after infection, with median 79 days (and mean days) diagnosis COVID-19. performed semi-structured interviews, neurological examinations, 3T-MRI scans, assessments. For MRI analyses, included non-infected 77 controls. The white matter (WM) investigation diffusion tensor images (DTI) functional connectivity resting-state (RS-fMRI). patients reported memory loss (36%), fatigue (31%) headache (29%). quantitative analyses confirmed (83% participants), excessive somnolence (35%), impaired phonemic verbal fluency (21%), categorical (13%) logical immediate recall (16%). WM DTI revealed higher axial diffusivity values post-infected compared to Compared controls, there were no significant differences the posterior cingulum cortex. There correlations between scores features RS-fMRI). Our results suggest persistent impairment subtle abnormalities depression symptoms. longitudinal will clarify whether these are temporary permanent.

Language: Английский

Citations

21

The Serotonin 1A (5-HT1A) Receptor as a Pharmacological Target in Depression DOI
Alexander L. W. Smith, Catherine J. Harmer, Philip J. Cowen

et al.

CNS Drugs, Journal Year: 2023, Volume and Issue: 37(7), P. 571 - 585

Published: June 29, 2023

Language: Английский

Citations

34

Glucocorticoids and cognitive function: a walkthrough in endogenous and exogenous alterations DOI Creative Commons
Dario De Alcubierre, Davide Ferrari, G Mauro

et al.

Journal of Endocrinological Investigation, Journal Year: 2023, Volume and Issue: 46(10), P. 1961 - 1982

Published: April 14, 2023

Abstract Purpose The hypothalamic–pituitary–adrenal (HPA) axis exerts many actions on the central nervous system (CNS) aside from stress regulation. Glucocorticoids (GCs) play an important role in affecting several cognitive functions through effects both glucocorticoid (GR) and mineralocorticoid receptors (MR). In this review, we aim to unravel spectrum of dysfunction secondary derangement circulating levels endogenous exogenous glucocorticoids. Methods All relevant human prospective retrospective studies published up 2022 PubMed reporting information HPA disorders, GCs, cognition were included. Results Cognitive impairment is commonly found GC-related disorders. main brain areas affected are hippocampus pre-frontal cortex, with memory being most domain. Disease duration, circadian rhythm disruption, GCs levels, unbalanced MR/GR activation all risk factors for decline these patients, albeit conflicting data among different conditions. Lack normalization after treatment potentially attributable GC-dependent structural alterations, which can persist even long-term remission. Conclusion recognition deficits patients disorders challenging, often delayed, or mistaken. Prompt underlying disease may be avoid a long-lasting impact GC-sensitive brain. However, resolution hormonal imbalance not always followed by complete recovery, suggesting irreversible adverse CNS, there no specific treatments. Further needed find mechanisms involved, eventually targeted strategies.

Language: Английский

Citations

30

Altered brain dynamic in major depressive disorder: state and trait features DOI Creative Commons
Nooshin Javaheripour, Lejla Čolić, Nils Opel

et al.

Translational Psychiatry, Journal Year: 2023, Volume and Issue: 13(1)

Published: July 17, 2023

Temporal neural synchrony disruption can be linked to a variety of symptoms major depressive disorder (MDD), including mood rigidity and the inability break cycle negative emotion or attention biases. This might imply that altered dynamic may play role in persistence exacerbation MDD symptoms. Our study aimed investigate changes whole-brain patterns brain functional connectivity activity related depression using hidden Markov model (HMM) on resting-state magnetic resonance imaging (rs-fMRI) data. We compared dynamics large sample 314 patients with (65.9% female; age (mean ± standard deviation): 35.9 13.4) 498 healthy controls (59.4% age: 34.0 12.8). The HMM was used explain variations rs-fMRI averaged across by set six unique recurring states. proportion time spent each state average duration visits assess stability between different groups. Compared controls, showed significantly higher proportional temporal characterized weak within all networks relatively strong regions located somatosensory motor (SMN), salience (SN), dorsal (DAN) networks. Both this associated severity. Healthy contrast group, but whole brain. These findings suggest disrupted is present current

Language: Английский

Citations

24

The involvement of neuroinflammation in an animal model of dementia and depression DOI

Gabriel Casagrande Zabot,

Eduarda Behenck Medeiros, Bárbara Machado Naspolini Macarini

et al.

Progress in Neuro-Psychopharmacology and Biological Psychiatry, Journal Year: 2024, Volume and Issue: 133, P. 110999 - 110999

Published: March 27, 2024

Language: Английский

Citations

13

Interventions of cognitive impairment in older adults: A comprehensive review DOI Creative Commons
Shivani Chib, Kajal Sharma,

Randhir Singh

et al.

Aging and Health Research, Journal Year: 2025, Volume and Issue: unknown, P. 100223 - 100223

Published: Feb. 1, 2025

Language: Английский

Citations

1

Psilocybin for dementia prevention? The potential role of psilocybin to alter mechanisms associated with major depression and neurodegenerative diseases DOI Creative Commons

Zarah R. Haniff,

Mariia Bocharova, Tim Mantingh

et al.

Pharmacology & Therapeutics, Journal Year: 2024, Volume and Issue: 258, P. 108641 - 108641

Published: April 6, 2024

Major depression is an established risk factor for subsequent dementia, and in late life may also represent a prodromal state of dementia. Considering current challenges the clinical development disease modifying therapies focus research shifting towards prevention modification factors to alter neurodegenerative trajectory. Understanding mechanistic commonalities underlying affective symptoms cognitive decline reveal biomarkers aid early identification those at progressing dementia during preclinical phase disease, thus allowing timely intervention. Adult hippocampal neurogenesis (AHN) phenomenon that describes birth new neurons dentate gyrus throughout it associated with spatial learning, memory mood regulation. Microglia are innate immune system macrophages central nervous carefully regulate AHN via multiple mechanisms. Disruption both major microgliosis hallmark several diseases. Emerging evidence suggests psychedelics promote neuroplasticity, including neurogenesis, be immunomodulatory. In this context, psilocybin, serotonergic agonist rapid-acting antidepressant properties has potential ameliorate intersecting pathophysiological processes relevant narrative review, we on base effects psilocybin adult microglial form function; which suggest modulate mechanisms action, have implications altering progression from risk.

Language: Английский

Citations

6

TAAR1 in dentate gyrus is involved in chronic stress-induced impairments in hippocampal plasticity and cognitive function DOI
Yue Zhang, Xianqiang Zhang,

Wei-Pan Niu

et al.

Progress in Neuro-Psychopharmacology and Biological Psychiatry, Journal Year: 2024, Volume and Issue: 132, P. 110995 - 110995

Published: March 19, 2024

Language: Английский

Citations

5

SSRIs in the Treatment of Depression: A Pharmacological CUL-DE-SAC? DOI
Philip J. Cowen

Current topics in behavioral neurosciences, Journal Year: 2023, Volume and Issue: unknown, P. 1 - 19

Published: Jan. 1, 2023

Language: Английский

Citations

9

Clinical practice guidelines on the assessment and management of cognitive impairment in major depressive disorder DOI Creative Commons

Om Prakash Singh,

Priya Ranjan Avinash,

Anita Gautam

et al.

Indian Journal of Psychiatry, Journal Year: 2025, Volume and Issue: 67(1), P. 98 - 105

Published: Jan. 1, 2025

INTRODUCTION Epidemiology Cognitive deficit is a trivialized symptom of most prevalent psychiatric condition called major depressive disorder (MDD).[1] With staggering global prevalence approximately 350 million, MDD contributes to significant loss in quality life and increased economic burden.[2] One or more cognitive faculties patients are adversely affected tend persist despite the remission episode [Figure 1].[3]Figure 1: Concise framework assessment management Cognition Subjects with Major Depressive DisorderUpon resolution episode, individual may show experience considerable improvement measures. but there still residual symptoms that continue exist. [Table 1].[4] The one has been reported be standard deviations below normative value, 25–50% subjects MDD.[4]Table domains disorderCognitive disorder: an epiphenomenon endophenotype Recent research suggests impairment depression accurately conceptualized as rather than merely epiphenomenon. As endophenotype, represent heritable trait increases vulnerability persists even during periods remission.[5] presence this create "double hit" effect, where underlying interacts neurotoxic effects episodes, potentially accelerating neurodegeneration increasing risk developing conditions such mild (MCI) dementia. This interplay between deficits vicious cycle, each exacerbating other over time, ultimately leading profound persistent neurocognitive impairments.[6] Aside from continuum, lies pseudodementia. reversible dementia-like phenomenon appears mood-cognition medius. Table 2 gives concise comparison phenotypes associated different conditions. mood cognition further gets complicated when iatrogenic factor takes wheel. mechanisms how psychotropics lead deterioration have presented 3.[7]Table 2: Comparison disorders lying on spectrumTable 3: Mechanisms psychotropic induced impairmentDissecting mdd phenotypic definition DSM5 (Diagnostic Statistical Manual 5) typology for includes discrete clinical as: melancholia, anxious distress, atypicality, psychotic features mixed features, those peripartum onset. Williams et al. 2013, took neural circuitry-based approach define biotypes 4].[13]Table 4: Different Biotypes Depression based circuitryAgainst prevailing belief, problems would automatically improve got better, mediation models improvements control directly influence reduction enhancement after treatment.[4] Course across various Previously we discussed involvement several 1] MDD. However, heterogeneity functioning points course independent treatment[14]Table 5 summarizes longitudinal change domains.Table 5: temporal evolution MDDNeurobiological underpinnings multisystem aberrancy starting at level genetic architecture evolving into myriad cascades. Various chronic proinflammatory neuroimmune axis alterations, advent any stressor, translate changes neurochemistry brain connectivity. leads shift "rational brain" towards "emotional/sensory brain." processing negative stimuli.[17] Predictors outcome line evidence regarding outcomes limited often mixed. While plethora studies incredible, duration investigating demographic age-related variables was short. 6 findings respective reviews predictors.[18,19]Table 6: good poor MDDThe existing qualitative patient-related measures held priority by large number mental healthcare professionals.[20] guideline aims provide evidence-based recommendations individuals disorders. OBJECTIVES To standardize disorder. once they achieve remission. outline strategies persisting achieved enhance awareness understanding among end users i.e., Psychiatrists health professionals. SCOPE intended use psychiatrists, psychologists, professionals involved care ASSESSMENT OF COGNITIVE IMPAIRMENT General evaluation 1]:Any setting undergoes preliminary which screens them psychopathology, its severity. presentation should fulfill ICD 10 DSM criteria, required reach diagnosis Neither these classifications mentions dysfunction phenotype. These guidelines used conjunction Clinical Practice Guidelines issued Indian Psychiatry Society general elderly population.[21,22]Evaluation features: A baseline entails ruling out illnesses. itself not primary pathology. Hence while it relevant exclusive same, empirical cognizant might predictive prognostic marker treatment functioning. widely scales HAM-D 21 MADRS items assessing symptomatology. insufficient information. Several screening tools validated indian population listed 7]. For comprehensive evaluation, prominent institutional bodies constructed application 8].Table 7: Screening cognitionTable 8: tests standardized populationCommon neuropsychological tests: Trail-making test Digit span Controlled oral word association Token Test Stroop Rey Complex figure Wisconsin Card Symbol digit modalities symbol substitution test: California Verbal Learning Test/Ray auditory Clock drawing Weschler Adult Intelligence Scale 4th edition (WAIS-IV) adaptation Other Not India yet Perceived Deficits Questionnaire-Depression (PDQ-D) 20: subjective 4 cognition, namely: attention/concentration, retrospective memory, prospective planning/organization.[3] Online computerized tests[3]: THINC-it® resource CANTAB: Cambridge Neuropsychological Automated Battery (CANTAB) computer-based system. MANAGEMENT There no way addressing challenges impairments In cognizance studied. 2].Figure Modalities crucial elements influencing outcomesA. Stand-alone adjunctive pharmacotherapy AntidepressantsThere randomized controlled trials (RCTs) NMAs comparing effect wide range antidepressants 9. Only Shilyansky 2016[24] Prado 2018[23], meta-analyses study focused conventional antidepressants. rest included multimodal agent Vortioxetine. three studies, Vortioxetine consistently outperformed common terms benefits.[26–29]Table 9: NMA (Network Meta Analyses) describing outcomes.Adjunctive atypical antipsychoticsThere only showed beneficial results executive continuous attention cognition. favoring addition aripiprazole antidepressants.[30] likely indirect stabilizing mood.[31]Non-conventional Drug therapies Ketamine/Eketamine modulates glutamate neurotransmission, can rapid antidepressant procognitive effects.[14–16] Concerns raised long-term modulator MDD.[32] Cholinesterase inhibitors, donepezil galantamine, shown their inhibitors found ameliorate subsyndromal dementia behavioral symptoms. function older adults inconsistent[33,34] Eugeroics: agents promote wakefulness modulating dopamine neurotransmitters. Few modafinil armodafinil depression, reduce fatigue, cognition.[34,35] Memantine, NMDAR antagonist, well established. RCT assessed efficacy adjunct memantine old delayed recall group.[23] Psychological treatments Remediation Therapy (CRT) intervention designed Components: Computerized Exercises: Patients engage structured tasks challenge processes. Strategy Training: Participants learn compensatory manage difficulties. Group Sessions: CRT involves group-based training foster social interaction support. tailored person's specific needs. It combined (e.g., psychotherapy, pharmacotherapy) treatment.[36] behavior (CBT):In meta-analysis Cristea (2015), CBT robust medium improving dysfunctional thinking depression. Its ability restructuring activation available evidence. were differences thoughts. More needed fully understand differential psychotherapies depression.[37,38]Other Psychotherapies: less extensive data psychological outcomes. Neurostimulation Transcranial Magnetic Stimulation (TMS): Individual report however montage used, stimulation intensity, pulse pattern.[39,40] practice therapeutic response rTMS neuropsychiatric mention supporting role relative outcome.[41] systematic review 58 faculties.[42] direct current (tDCS): Anodal tDCS usually applied left dorsolateral prefrontal cortex (DLPFC). Direct Current (tDCS) promising case-control conducted depressed patients. ELECT-TDCS, SELECT-TDCS, DepressionDC trial did corroborate findings.[43] Electroconvulsive (ECT): therapy (ECT) acute, short-term, functions speed, function, attention.[44] Studies suggest ECT achieving memory verbal recall.[45] important note vary factors age, premorbid intellectual gender, anesthetic technique used.[46] Therefore, alternate neurostimulation method recommended better outcomes[47] Vagus Nerve (VNS) Figure 3 illustrates bottom-up mechanism vagus-mediated enhancement. Through preclinical study, vagus nerve efficacious paired learning consolidation phase task.Figure Mechanism enhancementThere also superior transcutaneous Cervical VNS auricular VNS. Two open demonstrated diagnosed treatment-resistant depression.[48,49] within month, gradual improvement. sustained 12 months[48] Complementary Alternative medical (CAMTs): defined "a group diverse systems, practices, products generally considered part medicine." Mind–Body MedicineMindfulness-based stress (MBSR) mindfulness-based (MBCT) body at-least domain least symptomatology.[50] methodology inspecting uniform. Additionally, requires properly trained instructors administer treatment.Aerobic ExerciseA overall use. concluded optimal exercise parameters moderate-to-vigorous times per week, session 60 minutes, weeks less, complementary effective works especially medication inpatient settings.[51]Natural ProbioticsA 2019 performance psychobiotic Lactobacillus Plantarum 299v (LP299v) aligned decrease serum kynurenine levels.[52] improved episodic high doses probiotics.[53]Nootropics: Recombinant erythropoietin (EPO): double-blind, randomized, placebo-controlled, recombinant mood-independent manner.[27] potential novel nootropics: nootropics limited. Well-designed, large-scale RCTs investigate safety. describe benefits.[54] Minocycline Insulin Antidiabetic Agents Thiazolidinediones). S-Adenosyl Methionine (SAMe) Omega-3 Polyunsaturated Fatty Acids N-acetylcysteine (NAC) Curcumin Statins Coenzyme Q10 Gingko biloba extract EGb761.[55] rehabilitation: MDD, flexibility performing goal-directed activity. rehabilitation employs repetitive like working causing disrupted circuitry.[56] 2016 moderate size attention, Memory. two types: Strategy-based training: Personalising target faculty, example, inductive reasoning.[57] Process-based programmed entrain participant hierarchy cumulatively process. speed attentional breadth Task-switching training.[57] tasks: commonly Paced Auditory Serial Addition (PASAT), skills measuring PASAT abilities, Sommer al., metacognitive skills, maladaptive thought patterns (i.e., rumination), Moreover, Computer-based, arithmetic exercises, focus sequencing, intelligence quotient (IQ), increase psychosocial functioning, hippocampal frontotemporal MDD.[56] CONCLUSION much previously thought. observed both symptomatic recovery phases multidomain some being vulnerable others. Early detection watchful prompt all Based resources needs patient tailor-made include repeated detailed assessment. pharmacotherapy, alternative lifestyle management, neuromodulation combination resources. Financial support sponsorship Nil. Conflicts interest conflicts interest.

Language: Английский

Citations

0