Clinical Approaches to Late-Onset Psychosis

Kim, Ki-Won; Jeon, Hong Jin; Myung, Woo Jae; Suh, Seung Wan; Seong, Sang Cheol; Hwang, Jae Yeon; Ryu, Je Il; Park, Seon Cheol

doi:10.3390/jpm12030381

Cited by 5 publications

(2 citation statements)

References 64 publications

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“…En las psicosis de comienzo tardío se describen alucinaciones en varias modalidades sensoriales, aparte las clásicas alucinaciones auditivas de la esquizofrenia y suelen ser de índole más paranoide. También se objetivan ideación delirante y escasos trastornos de la esfera afectiva, aunque éstos pueden estar ausentes (Kim et al, 2022).…”

Section: Clínicaunclassified

Psicosis tardías y fenocopias

Ollari,

Deschle,

Rubiño

et al. 2023

Vertex Rev Arg Psiquiatr

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Los síntomas psicóticos pueden manifestarse a cualquier edad, pero en las personas mayores representan un verdadero desafío diagnóstico. Pueden observarse trastornos del pensamiento, alucinaciones (usualmente visuales), trastornos del estado de ánimo con ideas delirantes, trastornos en la interacción social y ocasionalmente agresividad verbal o física (Karon & VandenBos, 1998). Desde lasprimeras descripciones de la psiquiatría clásica se ha intentado definir a las psicosis observadas en las personas mayores y determinar si se trata de síndromes “psiquiátricos” primarios o, por el contrario, si se los puede atribuir a otras patologías. Así, han surgido diferentes conceptos, como psicosis de comienzo tardío (Late Onset Psychosis) o esquizofrenia de comienzo tardío (Late-Onset Schizophrenia – LOS), psicosis de comienzo muy tardío (Very Late-Onset Psychosis)o psicosis esquizofreniforme de comienzo muy tardío (very late-onset schizophrenia-like psychosis – VLOSL), psicosis de la vida avanzada (Late-Life Psychosis), etc.

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Section: Clínicaunclassified

Psicosis tardías y fenocopias

Ollari,

Deschle,

Rubiño

et al. 2023

Vertex Rev Arg Psiquiatr

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“…There is extensive literature evidence on the underlying mechanisms and genetic architecture of NPSs in patients with clinically manifested neurodegenerative diseases, such as AD dementia, Parkinson’s disease (PD), Lewy body dementia (LBD), and frontotemporal dementia (FTD) [ 16 ]. Among older individuals with normal cognition, most genetic studies on psychiatric symptoms have focused on diagnosed psychiatric diseases, such as late-onset schizophrenia and delusional disorder [ 17 ]. However, the clinical features and underlying pathophysiology of psychiatric diseases differ from that of NPSs in AD and other neurodegenerative diseases.…”

Section: Introductionmentioning

confidence: 99%

Exploring the Genetic Landscape of Mild Behavioral Impairment as an Early Marker of Cognitive Decline: An Updated Review Focusing on Alzheimer’s Disease

Angelopoulou,

Koros,

Hatzimanolis

et al. 2024

IJMS

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The clinical features and pathophysiology of neuropsychiatric symptoms (NPSs) in dementia have been extensively studied. However, the genetic architecture and underlying neurobiological mechanisms of NPSs at preclinical stages of cognitive decline and Alzheimer’s disease (AD) remain largely unknown. Mild behavioral impairment (MBI) represents an at-risk state for incident cognitive impairment and is defined by the emergence of persistent NPSs among non-demented individuals in later life. These NPSs include affective dysregulation, decreased motivation, impulse dyscontrol, abnormal perception and thought content, and social inappropriateness. Accumulating evidence has recently begun to shed more light on the genetic background of MBI, focusing on its potential association with genetic factors related to AD. The Apolipoprotein E (APOE) genotype and the MS4A locus have been associated with affective dysregulation, ZCWPW1 with social inappropriateness and psychosis, BIN1 and EPHA1 with psychosis, and NME8 with apathy. The association between MBI and polygenic risk scores (PRSs) in terms of AD dementia has been also explored. Potential implicated mechanisms include neuroinflammation, synaptic dysfunction, epigenetic modifications, oxidative stress responses, proteosomal impairment, and abnormal immune responses. In this review, we summarize and critically discuss the available evidence on the genetic background of MBI with an emphasis on AD, aiming to gain insights into the potential underlying neurobiological mechanisms, which till now remain largely unexplored. In addition, we propose future areas of research in this emerging field, with the aim to better understand the molecular pathophysiology of MBI and its genetic links with cognitive decline.

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Serum Interleukin-6 in Schizophrenia: Associations with Clinical and Sociodemographic Characteristics

Zhilyaeva,

Rukavishnikov,

Manakova

et al. 2023

Consortium Psychiatricum

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BACKGROUND:Recentlyasignificant part of schizophrenia studies have been focused on the role of cytokines, especially interleukin-6 (IL-6). Some authors have suggestedapathogenetic role for IL-6 in schizophrenia and concluded that therapy that centers on suppressing IL-6 activity may prove beneficial for certain categories of patients with the disorder. However, many questions about whether the changes in IL-6 levels in schizophrenia are primary, related to symptoms or caused by therapy, are concomitant metabolic disorders, are related to smoking or other secondary factors remain unanswered. AIM:To assess the level of serum IL-6 in patients with schizophrenia in comparison with healthy controls, as well as to study its association with clinical and socio-demographic characteristics. METHODS:Some 125 patients with schizophrenia and 95 healthy volunteers were examined.Theevaluation of IL-6 was performed by enzyme immunoassay. All patients were assessed using standardized psychometric instruments. Information from patient medical records on the course of the disease and treatment wasanalyzed. RESULTS:Thelevel of IL-6 was significantly higher in the patients than in the healthy volunteers (z=2.58;p=0.0099), but among men the difference between the patients and volunteers was not significant. Statistically significant correlations were found between the level of serum IL-6 and the severity of the cognitive impairment of patients: (auditory [ρ=–0.31;p=0.00063] and working memory [ρ=−0.25;p=0.0065], hand-eye coordination [ρ=−0.29;p=0.0011], verbal fluency [ρ=−0.28;p=0.0019] and problem-solving capacity [ρ=−0.22;p=0.013]), total severity of schizophrenia symptoms (PANSS, ρ=0.22;p=0.016), PANSS positive subscale (ρ=0.18;p=0.048), and the age of manifestation (ρ=0.20;p=0.025) and disease duration (ρ=0.18;p=0.043).Thelevel of IL-6 was the lowest in patients treated with third-generation antipsychotics, and the highest in those treated withfirst-generation antipsychotics (H=6.36;p=0.042). Moreover, in hospital patients, the level of IL-6 was significantly higher than in outpatients and inpatients hospitals (H=18.59;p=0.0001). CONCLUSION:Thestudy confirmed that there are associations between the serum IL-6 level and schizophrenia, the age of the patient, duration of the disease and how late in one's life cycle it began manifesting itself, as well asanumber of clinical characteristics. Considering that IL-6isassociated withawide range of symptoms that are loosely controlled by antipsychotics, this biochemical marker needs to be studied to look into how closely its level tracks with an unfavorable course of schizophrenia. That would require further prospective studies.

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Clinical Approaches to Late-Onset Psychosis

Cited by 5 publications

References 64 publications

Psicosis tardías y fenocopias

Psicosis tardías y fenocopias

Exploring the Genetic Landscape of Mild Behavioral Impairment as an Early Marker of Cognitive Decline: An Updated Review Focusing on Alzheimer’s Disease

Serum Interleukin-6 in Schizophrenia: Associations with Clinical and Sociodemographic Characteristics

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