RESUMEN
Importance: Art therapy has a long-standing tradition in patient treatment. As scientific interest in its use has recently grown, a comprehensive assessment of active visual art therapy is crucial to understanding its potential benefits. Objective: To assess the association of active visual art therapy with health outcomes across patient groups and comparators. Data Sources: The systematic literature search included the Cochrane Library, Embase, MEDLINE, CINAHL, ERIC, American Psychological Association PsycArticles, American Psychological Association PsycInfo, PSYNDEX, the German Clinical Trials Register, and ClinicalTrials.gov. No filters regarding language were applied. The search covered all dates before March 2021. Data analysis was conducted from April 24 to September 8, 2023. Study Selection: Randomized clinical trials with any type of patient population comparing the intervention with any control not using active visual art therapy were included. Two researchers independently screened the abstracts and full texts. Data Extraction and Synthesis: Data extraction followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, and study quality was evaluated using the Cochrane Risk of Bias tool. Data were synthesized using narrative summaries, forest plots, and random effects meta-analyses. Main Outcome and Measures: In line with the protocol, all outcome measures of the included studies were extracted. Results: The search identified 3104 records, of which 356 outcomes of 69 studies were included, with a total of approximately 4200 participants, aged 4 to 96 years, in the review. The meta-analyses included 50 studies and 217 outcomes of 2766 participants. Treatment indications included mental, neurological, and other somatic disorders, and prevention. Most outcome measures focused on depression, anxiety, self-esteem, social adjustment, and quality of life. Art therapy was associated with an improvement in 18% of the 217 outcomes compared with the controls (1%), while 81% showed no improvement. The standardized mean difference in the change from baseline of the meta-analyses of 0.38 (95% CI, 0.26-0.51) and posttest analysis of 0.19 (95% CI, 0.12-0.26) also indicated an improvement of outcomes associated with art therapy. Overall study quality was low. Conclusions and Relevance: In this systematic review and meta-analysis of randomized clinical trials, visual art therapy was associated with therapeutic benefits for some outcomes, although most studies were of low quality. Further good-quality studies are needed to provide additional insights for its best possible integration into routine care.
Asunto(s)
Arteterapia , Humanos , Arteterapia/métodos , Adulto , Calidad de Vida/psicología , Masculino , Femenino , Ensayos Clínicos Controlados Aleatorios como Asunto , Adolescente , Resultado del Tratamiento , Anciano , Evaluación de Resultado en la Atención de SaludRESUMEN
BACKGROUND: Environmental factors are critical in the development of age-related cognitive decline and dementia. A western diet (WD) can cause nutrient deficiency and inflammation that could impact cognition directly. It is increasingly recognized that innate immune responses by brain myeloid cells, such as resident microglia, and infiltrating peripheral monocytes/macrophages may represent an essential link between a WD, cognitive decline, and dementia. Our previous data demonstrated that chronic consumption of a WD induced inflammation through brain myeloid cells in aging mice and a mouse model of Alzheimer's disease (AD). However, the subtypes of myeloid cells that contribute to the WD-induced inflammation remain unclear. METHODS: C57BL/6J (B6), myeloid cell reporter mice (B6.Ccr2RFP/+Cx3cr1GFP/+), and Ccr2-deficient mice (B6.Ccr2RFP/RFP) were fed a WD or a control chow diet (CD) from 2 to 6 or 12 months of age. CD11b+CD45lo and CD11b+CD45hi cells from WD- and CD-fed B6 or Ccr2-deficient mice were characterized using flow cytometry, RNA-sequencing, and immunofluorescence. RESULTS: Ccr2::RFP expressing myeloid cells were significantly increased in brains of WD- compared to CD-fed mice, but were not elevated in Ccr2-deficient WD-fed mice. The percent of CD11b+CD45hi cells was significantly increased in WD- compared to CD-fed mice. Comparison of RNA-sequencing data with immune cell data in ImmGen supports that CD11b+CD45hi cells from WD-fed mice are enriched for peripheral monocytes and neutrophils. Ingenuity pathway analysis predicted these cells elicit proinflammatory responses that may be damaging to the brain. Using stringent criteria for gene expression levels between CD11b+CD45hi and CD11b+CD45lo cells, we identified approximately 70 genes that we predict are uniquely expressed in infiltrating cells, including Itgal, Trem1, and Spp1 (osteopontin, OPN). Finally, we show a significantly greater number of OPN+IBA1- cells in WD- compared to CD-fed mice that we propose are activated neutrophils based on ImmGen data. OPN+IBA1- cells are not significantly increased in Ccr2-deficient WD-fed mice. CONCLUSIONS: These data further support the model that peripheral myeloid cells enter the brain in response to diet-induced obesity. Elucidating their contribution to age-related cognitive decline and age-related neurodegenerative diseases should offer new avenues for therapeutic intervention in Alzheimer's disease and related dementias, where diet/obesity are major risk factors.
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Antígeno CD11a/metabolismo , Dieta Occidental/efectos adversos , Perfilación de la Expresión Génica/métodos , Obesidad/metabolismo , Osteopontina/metabolismo , Receptor Activador Expresado en Células Mieloides 1/metabolismo , Animales , Encéfalo/metabolismo , Femenino , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Transgénicos , Células Mieloides/metabolismo , Obesidad/inducido químicamente , Obesidad/genética , Osteopontina/genética , Receptor Activador Expresado en Células Mieloides 1/genéticaRESUMEN
Obesity in the western world has reached epidemic proportions, and yet the long-term effects on brain health are not well understood. To address this, we performed transcriptional profiling of brain regions from a mouse model of western diet (WD)-induced obesity. Both the cortex and hippocampus from C57BL/6J (B6) mice fed either a WD or a control diet from 2 months of age to 12 months of age (equivalent to midlife in a human population) were profiled. Gene set enrichment analyses predicted that genes involved in myelin generation, inflammation, and cerebrovascular health were differentially expressed in brains from WD-fed compared to control diet-fed mice. White matter damage and cerebrovascular decline were evident in brains from WD-fed mice using immunofluorescence and electron microscopy. At the cellular level, the WD caused an increase in the numbers of oligodendrocytes and myeloid cells suggesting that a WD is perturbing myelin turnover. Encouragingly, cerebrovascular damage and white matter damage were prevented by exercising WD-fed mice despite mice still gaining a significant amount of weight. Collectively, these data show that chronic consumption of a WD in B6 mice causes obesity, neuroinflammation, and cerebrovascular and white matter damage, but these potentially damaging effects can be prevented by modifiable risk factors such as exercise.
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Disfunción Cognitiva/etiología , Disfunción Cognitiva/prevención & control , Ejercicio Físico/fisiología , Leucoencefalopatías/prevención & control , Obesidad/complicaciones , Condicionamiento Físico Animal/fisiología , Animales , Humanos , Inflamación , Leucoencefalopatías/patología , Ratones Endogámicos C57BL , Obesidad/prevención & control , Oligodendroglía/patología , Sustancia Blanca/citología , Sustancia Blanca/patologíaRESUMEN
Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-ß (Aß) peptide is central to AD; however, evidence in humans and animals suggests that Aß buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aß toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB(Tg)) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB(Tg) mice that carry only one copy of Meox2 (B6.APB(Tg).Mx(-/+)) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB(Tg) mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD.