Histidine modulates amyloid-like assembly of peptide nanomaterials and confers enzyme-like activity.

Amyloid-like assembly is not only associated with pathological events, but also leads to the development of novel nanomaterials with unique properties. Herein, using Fmoc diphenylalanine peptide (Fmoc-F-F) as a minimalistic model, we found that histidine can modulate the assembly behavior of Fmoc-F-F and induce enzyme-like catalysis. Specifically, the presence of histidine rearranges the ß structure of Fmoc-F-F to assemble nanofilaments, resulting in the formation of active site to mimic peroxidase-like activity that catalyzes ROS generation. A similar catalytic property is also observed in Aß assembled filaments, which is correlated with the spatial proximity between intermolecular histidine and F-F. Notably, the assembled Aß filaments are able to induce cellular ROS elevation and damage neuron cells, providing an insight into the pathological relationship between Aß aggregation and Alzheimer's disease. These findings highlight the potential of histidine as a modulator in amyloid-like assembly of peptide nanomaterials exerting enzyme-like catalysis.

Bisphosphonate-incorporated coatings for orthopedic implants functionalization.

Bisphosphonates (BPs), the stable analogs of pyrophosphate, are well-known inhibitors of osteoclastogenesis to prevent osteoporotic bone loss and improve implant osseointegration in patients suffering from osteoporosis. Compared to systemic administration, BPs-incorporated coatings enable the direct delivery of BPs to the local area, which will precisely enhance osseointegration and bone repair without the systemic side effects. However, an elaborate and comprehensive review of BP coatings of implants is lacking. Herein, the cellular level (e.g., osteoclasts, osteocytes, osteoblasts, osteoclast precursors, and bone mesenchymal stem cells) and molecular biological regulatory mechanism of BPs in regulating bone homeostasis are overviewed systematically. Moreover, the currently available methods (e.g., chemical reaction, porous carriers, and organic material films) of BP coatings construction are outlined and summarized in detail. As one of the key directions, the latest advances of BP-coated implants to enhance bone repair and osseointegration in basic experiments and clinical trials are presented and critically evaluated. Finally, the challenges and prospects of BP coatings are also purposed, and it will open a new chapter in clinical translation for BP-coated implants.

Organ Crosstalk Contributes to Muscle Wasting in Chronic Kidney Disease.

Muscle wasting (ie, atrophy) is a serious consequence of chronic kidney disease (CKD) that reduces muscle strength and function. It reduces the quality of life for CKD patients and increases the risks of comorbidities and mortality. Current treatment strategies to prevent or reverse skeletal muscle loss are limited owing to the broad and systemic nature of the initiating signals and the multifaceted catabolic mechanisms that accelerate muscle protein degradation and impair protein synthesis and repair pathways. Recent evidence has shown how organs such as muscle, adipose, and kidney communicate with each other through interorgan exchange of proteins and RNAs during CKD. This crosstalk changes cell functions in the recipient organs and represents an added dimension in the complex processes that are responsible for muscle atrophy in CKD. This complexity creates challenges for the development of effective therapies to ameliorate muscle wasting and weakness in patients with CKD.

Tumor necrosis factor-like cytokine 1A plays a role in inflammatory bowel disease pathogenesis.

The binding of tumor necrosis factor-like cytokine 1A (TL1A) to death receptor 3 (DR3) plays an important role in the interaction between dendritic cells (DCs) and T cells and contributes to intestinal inflammation development. However, the mechanism by which DCs expressing TL1A mediate helper T (Th) cell differentiation in the intestinal lamina propria (LP) during the pathogenesis of inflammatory bowel disease remains unclear. In this study, we found that TL1A/DR3 promoted Th1 and Th17 cell differentiation in T-T and DC-T cell interaction-dependent manners. TL1A-deficient CD4+ T cells failed to polarize into Th1/Th17 cells and did not cause colonic inflammation in a T cell transfer colitis model. Notably, TL1A was located in the cytoplasm and nuclei of DCs, positively regulated the DC-specific ICAM-grabbing nonintegrin/RAF1/nuclear factor κB signaling pathway, enhanced the antigen uptake ability of DCs, and promoted TLR4-mediated DC activation, inducing naive CD4+ T cell differentiation into Th1 and Th17 cells. Our work reveals that TL1A plays a regulatory role in inflammatory bowel disease pathogenesis.

Autophagy counters inflammation-driven glycolytic impairment in aging hematopoietic stem cells.

Aging of the hematopoietic system promotes various blood, immune and systemic disorders and is largely driven by hematopoietic stem cell (HSC) dysfunction ( 1 ). Autophagy is central for the benefits associated with activation of longevity signaling programs ( 2 ), and for HSC function and response to nutrient stress ( 3,4 ). With age, a subset of HSCs increases autophagy flux and preserves some regenerative capacity, while the rest fail to engage autophagy and become metabolically overactivated and dysfunctional ( 4 ). However, the signals that promote autophagy in old HSCs and the mechanisms responsible for the increased regenerative potential of autophagy-activated old HSCs remain unknown. Here, we demonstrate that autophagy activation is an adaptive survival response to chronic inflammation in the aging bone marrow (BM) niche ( 5 ). We find that inflammation impairs glucose metabolism and suppresses glycolysis in aged HSCs through Socs3-mediated impairment of AKT/FoxO-dependent signaling. In this context, we show that inflammation-mediated autophagy engagement preserves functional quiescence by enabling metabolic adaptation to glycolytic impairment. Moreover, we demonstrate that transient autophagy induction via a short-term fasting/refeeding paradigm normalizes glucose uptake and glycolytic flux and significantly improves old HSC regenerative potential. Our results identify inflammation-driven glucose hypometabolism as a key driver of HSC dysfunction with age and establish autophagy as a targetable node to reset old HSC glycolytic and regenerative capacity. One-Sentence Summary: Autophagy compensates for chronic inflammation-induced metabolic deregulation in old HSCs, and its transient modulation can reset old HSC glycolytic and regenerative capacity.

Nitroalkanes as thioacyl equivalents to access thioamides and thiopeptides.

Thioamides are an important, but a largely underexplored class of amide bioisostere in peptides. Replacement of oxoamide units with thioamides in peptide therapeutics is a valuable tactic to improve biological activity and resistance to enzymatic hydrolysis. This tactic, however, has been hampered by insufficient methods to introduce thioamide bonds into peptide or protein backbones in a site-specific and stereo-retentive fashion. In this work, we developed an efficient and mild thioacylation method to react nitroalkanes with amines directly in the presence of elemental sulfur and sodium sulfide to form a diverse range of thioamides in high yields. Notably, this convenient method can be employed for the controlled thioamide coupling of multifunctionalized peptides without epimerization of stereocenters, including the late stage thioacylation of advanced compounds of biological and medicinal interest. Experimental interrogation of postulated mechanisms currently supports the intermediacy of thioacyl species.

Comparative analyses of the effects of sublethal doses of emamectin benzoate and tetrachlorantraniliprole on the gut microbiota of Spodoptera frugiperda (Lepidoptera: Noctuidae).

Spodoptera frugiperda (J. E. Smith) is an important invasive pest that poses a serious threat to global crop production. Both emamectin benzoate (EB) and diamide insecticides are effective insecticides used to protect against S. frugiperda. Here, 16S rRNA sequencing was used to characterize the gut microbiota in S. frugiperda larvae exposed to EB or tetrachlorantraniliprole (TE). Firmicutes and Proteobacteria were found to be the dominant bacterial phyla present in the intestines of S. frugiperda. Following insecticide treatment, larvae were enriched for species involved in the process of insecticide degradation. High-level alpha and beta diversity indices suggested that exposure to TE and EB significantly altered the composition and diversity of the gastrointestinal microbiota in S. frugiperda. At 24 h post-EB treatment, Burkholderia-Caballeronia-Paraburkholderia abundance was significantly increased relative to the control group, with significant increases in Stenotrophobacter, Nitrospira, Blastocatella, Sulfurifustis, and Flavobacterium also being evident in these larvae. These microbes may play a role in the degradation or detoxification of EB and TE, although further work will be needed to explore the mechanisms underlying such activity. Overall, these findings will serve as a theoretical foundation for subsequent studies of the relationship between the gut microbiota and insecticide resistance in S. frugiperda (J. E. Smith) (Lepidoptera: Noctuidae).

Dual-targeting inhibition of TNFR1 for alleviating rheumatoid arthritis by a novel composite nucleic acid nanodrug.

Selective suppression of tumor necrosis factor (TNF) α-TNF receptor 1 (TNFR1) signaling is a potent solution for rheumatoid arthritis (RA). Herein, novel composite nucleic acid nanodrugs that simultaneously restrain TNF α binding and TNFR1 multimerization were designed to reinforce inhibition of TNF α-TNFR1 signaling for RA therapy. Towards this end, a novel peptide Pep4-19 that suppresses TNFR1 clustering was extracted from TNFR1. The resulting peptide and a DNA aptamer Apt2-55, which inhibits TNF α binding, were integrally or separately anchored on DNA tetrahedron (TD) to obtain nanodrugs with different spatial distribution of Apt2-55 and Pep4-19 (TD-3A-3P and TD-3(A-P)). Our results showed that Pep4-19 enhanced the viability of inflammatory L929 cells. Both TD-3A-3P and TD-3(A-P) suppressed caspase 3, reduced cell apoptosis, and inhibited FLS-RA migration. Compared to TD-3(A-P), TD-3A-3P supplied sufficient flexibility for Apt2-55 and Pep4-19, and showed better anti-inflammation properties. Furthermore, TD-3A-3P significantly relieved symptoms in collagen-induced arthritis (CIA) mice, and the anti-RA efficacy through intravenous injection was comparable to transdermal administration via microneedles. Overall, the work provides an effective strategy for RA treatment by dual-targeting TNFR1, and demonstrates that microneedles are promising approach to drug administration in the treatment of RA.

Immune microenvironment analysis and novel biomarkers of early-stage lung adenocarcinoma evolution.

Background: Lung cancer is the deadliest and most diagnosed type of cancer worldwide. The 5-year survival rate of lung adenocarcinoma (LUAD) dropped significantly when tumor stages advanced. Patients who received surgically resecting at the pre-invasive stage had a 5-year survival rate of nearly 100%. However, the study on the differences in gene expression profiles and immune microenvironment among pre-invasive LUAD patients is still lacking. Methods: In this study, the gene expression profiles of three pre-invasive LUAD stages were compared using the RNA-sequencing data of 10 adenocarcinoma in situ (AIS) samples, 12 minimally invasive adenocarcinoma (MIA) samples, and 10 invasive adenocarcinoma (IAC) samples. Results: The high expression levels of PTGFRN (Hazard Ratio [HR] = 1.45; 95% Confidence Interval [CI]: 1.08-1.94; log-rank P = 0.013) and SPP1 (HR = 1.44; 95% CI: 1.07-1.93; log-rank P = 0.015) were identified to be associated with LUAD prognosis. Moreover, the early LUAD invasion was accompanied by the enhancement of antigen presentation ability, reflected by the increase of myeloid dendritic cells infiltration rate (Cuzick test P < 0.01) and the upregulation of seven important genes participating in the antigen presentation, including HLA-A (Cuzick test P = 0.03), MICA (Cuzick test P = 0.01), MICB (Cuzick test P = 0.01), HLA-DPA1 (Cuzick test P = 0.04), HLA-DQA2 (Cuzick test P < 0.01), HLA-DQB1 (Cuzick test P = 0.03), and HLA-DQB2 (Cuzick test P < 0.01). However, the tumor-killing ability of the immune system was inhibited during this process, as there were no rising cytotoxic T cell activity (Cuzick test P = 0.20) and no increasing expression in genes encoding cytotoxic proteins. Conclusion: In all, our research elucidated the changes in the immune microenvironment during early-stage LUAD evolution and may provide a theoretical basis for developing novel early-stage lung cancer therapeutic targets.

Environmental concentrations of surfactants as a trigger for climax of horizonal gene transfer of antibiotic resistance.

Ubiquitous antibiotic resistance genes (ARGs) is a significant global human health concern. Surfactants have been extensively used worldwide, and the consumption of surfactants containing hygiene, cleaning agents and disinfectants was multiplied during COVID-19 pandemic, which have caused significantly increased pollution of surfactants in aquatic environment. Whether such ever-increasing surfactant concentration boost dissemination risk of ARGs still remains unknown. Here the effects of three typical surfactants such as sodium dodecyl sulfate, cetyltrimethylammonium bromide and benzalkonium chloride on the transformation of pUC19 plasmid (2686 bp)-borne ARGs to recipient bacteria E. coli DH5ɑ were investigated. It was found that these surfactants at environmental concentrations facilitated horizonal gene transfer (HGT) via transformation. The transformation triggering concentrations for the three surfactants were 0.25-0.34 mg/L with a maximum increased transformation frequency of 13.51-22.93-fold. The mechanisms involved in activated HGT of ARGs via transformation triggered by surfactants could be mainly attributed to the increased production of reactive oxygen species, which further enhanced cell membrane permeability. These findings provide new sights for understanding of ARG propagation and also imply that the drastic rise of surfactant concentration in aquatic environment may significantly increase the dissemination risk of antibiotic resistance.

Strong succession in prokaryotic association networks and community assembly mechanisms in an acid mine drainage-impacted riverine ecosystem.

Acid mine drainage (AMD) serves as an ideal model system for investigating microbial ecology, interaction, and assembly mechanism in natural environments. While previous studies have explored the structure and function of microbial communities in AMD, the succession patterns of microbial association networks and underlying assembly mechanisms during natural attenuation processes remain elusive. Here, we investigated prokaryotic microbial diversity and community assembly along an AMD-impacted river, from the extremely acidic, heavily polluted headwaters to the nearly neutral downstream sites. Microbial diversity was increased along the river, and microbial community composition shifted from acidophile-dominated to freshwater taxa-dominated communities. The complexity and relative modularity of the microbial networks were also increased, indicating greater network stability during succession. Deterministic processes, including abiotic selection of pH and high contents of sulfur and iron, governed community assembly in the headwaters. Although the stochasticity ratio was increased downstream, manganese content, microbial negative cohesion, and relative modularity played important roles in shaping microbial community structure. Overall, this study provides valuable insights into the ecological processes that govern microbial community succession in AMD-impacted riverine ecosystems. These findings have important implications for in-situ remediation of AMD contamination.

Endurance Exercise-Induced Fgf21 Promotes Skeletal Muscle Fiber Conversion through TGF-ß1 and p38 MAPK Signaling Pathway.

Fgf21 has been identified as playing a regulatory role in muscle growth and function. Although the mechanisms through which endurance training regulates skeletal muscle have been widely studied, the contribution of Fgf21 remains poorly understood. Here, muscle size and function were measured, and markers of fiber type were evaluated using immunohistochemistry, immunoblots, or qPCR in endurance-exercise-trained wild-type and Fgf21 KO mice. We also investigated Fgf21-induced fiber conversion in C2C12 cells, which were incubated with lentivirus and/or pathway inhibitors. We found that endurance exercise training enhanced the Fgf21 levels of liver and GAS muscle and exercise capacity and decreased the distribution of skeletal muscle fiber size, and fast-twitch fibers were observed converting to slow-twitch fibers in the GAS muscle of mice. Fgf21 promoted the markers of fiber-type transition and eMyHC-positive myotubes by inhibiting the TGF-ß1 signaling axis and activating the p38 MAPK signaling pathway without apparent crosstalk. Our findings suggest that the transformation and function of skeletal muscle fiber types in response to endurance training could be mediated by Fgf21 and its downstream signaling pathways. Our results illuminate the mechanisms of Fgf21 in endurance-exercise-induced fiber-type conversion and suggest a potential use of Fgf21 in improving muscle health and combating fatigue.

Causal Associations of Air Pollution With Cardiovascular Disease and Respiratory Diseases Among Elder Diabetic Patients.

Extensive researches have linked air pollutants with cardiovascular disease (CVD) and respiratory diseases (RD), however, there is limited evidence on causal effects of air pollutants on morbidity of CVD or RD with comorbidities, particularly diabetes mellitus in elder patients. We included hospital admissions for CVD or RD among elder (≥65 years) diabetic patients between 2014 and 2019 in Beijing. A time-stratified case-crossover design based on negative-control exposure was used to assess causal associations of short-term exposure to air pollutants with CVD and RD among diabetic patients with the maximum lag of 7 days. A random forest regression model was used to calculate the contribution magnitude of air pollutants. A total of 493,046 hospital admissions were recorded. Per 10 µg/m3 uptick in PM1, PM2.5, PM10, SO2, NO2, O3, and 1 mg/m3 in CO was associated with 0.29 (0.05, 0.53), 0.14 (0.02, 0.26), 0.06 (0.00, 0.12), 0.36 (0.01, 0.70), 0.21 (0.02, 0.40), -0.08 (-0.25, 0.09), and 4.59 (0.56, 8.61) causal effect estimator for admission of CVD among diabetic patients, corresponding to 0.12 (0.05, 0.18), 0.09 (0.05, 0.13), 0.05, 0.23 (0.06, 0.41), 0.10 (0.02, 0.19), -0.04 (-0.06, -0.01), and 3.91(1.81, 6.01) causal effect estimator for RD among diabetic patients. The effect of gaseous pollutants was higher than particulate pollutants in random forest model. Short-term exposure to air pollution was causally associated with increased admission of CVD and RD among elder diabetic patients. Gaseous pollutants had a greater contribution to CVD and RD among elder diabetic patients.

Microbial community composition and degradation potential of petroleum-contaminated sites under heavy metal stress.

Total petroleum hydrocarbons (n-alkanes), semi-volatile organic compounds, and heavy metals pose major ecological risks at petrochemical-contaminated sites. The efficiency of natural remediation in situ is often unsatisfactory, particularly under heavy metal pollution stress. This study aimed to verify the hypothesis that after long-term contamination and restoration, microbial communities in situ exhibit significantly different biodegradation efficiencies under different concentrations of heavy metals. Moreover, they determine the appropriate microbial community to restore the contaminated soil. Therefore, we investigated the heavy metals in petroleum-contaminated soils and observed that heavy metals effects on distinct ecological clusters varied significantly. Finally, alterations in the native microbial community degradation ability were demonstrated through the occurrence of petroleum pollutant degradation function genes in different communities at the tested sites. Furthermore, structural equation modeling (SEM) was used to explain the influence of all factors on the degradation function of petroleum pollution. These results suggest that heavy metal contamination from petroleum-contaminated sites reduces the efficiency of natural remediation. In addition, it infers that MOD1 microorganisms have greater degradation potential under heavy metal stress. Utilizing appropriate microorganisms in situ may effectively help resist the stress of heavy metals and continuously degrade petroleum pollutants.

AI for Nanomaterials Development in Clean Energy and Carbon Capture, Utilization and Storage (CCUS).

Zero-carbon energy and negative emission technologies are crucial for achieving a carbon neutral future, and nanomaterials have played critical roles in advancing such technologies. More recently, due to the explosive growth in data, the adoption and exploitation of artificial intelligence (AI) as part of the materials research framework have had a tremendous impact on the development of nanomaterials. AI has enabled revolutionary next-generation paradigms to significantly accelerate all stages of material discovery and facilitate the exploration of the enormous design space. In this review, we summarize recent advancements of AI applications in nanomaterials discovery, with a special emphasis on the selected applications of AI and nanotechnology for the net-zero emission future including the development of solar cells, hydrogen energy, battery materials for renewable energy, and CO2 capture and conversion materials for carbon capture, utilization and storage (CCUS) technologies. In addition, we discuss the limitations and challenges of current AI applications in this area by identifying the gaps that exist in current development. Finally, we present the prospect for future research directions in order to facilitate the large-scale applications of artificial intelligence for advancements in nanomaterials.

Genotoxic aldehyde stress prematurely ages hematopoietic stem cells in a p53-driven manner.

Aged hematopoietic stem cells (HSCs) display diminished self-renewal and a myeloid differentiation bias. However, the drivers and mechanisms that underpin this fundamental switch are not understood. HSCs produce genotoxic formaldehyde that requires protection by the detoxification enzymes ALDH2 and ADH5 and the Fanconi anemia (FA) DNA repair pathway. We find that the HSCs in young Aldh2-/-Fancd2-/- mice harbor a transcriptomic signature equivalent to aged wild-type HSCs, along with increased epigenetic age, telomere attrition, and myeloid-biased differentiation quantified by single HSC transplantation. In addition, the p53 response is vigorously activated in Aldh2-/-Fancd2-/- HSCs, while p53 deletion rescued this aged HSC phenotype. To further define the origins of the myeloid differentiation bias, we use a GFP genetic reporter to find a striking enrichment of Vwf+ myeloid and megakaryocyte-lineage-biased HSCs. These results indicate that metabolism-derived formaldehyde-DNA damage stimulates the p53 response in HSCs to drive accelerated aging.

CEST 2022-three-dimensional amide proton transfer (APT) imaging can identify the changes of cerebral cortex in Parkinson's disease.

PURPOSE: Amide proton transfer (APT) imaging has shown its diagnostic and predictive superiority in Parkinson's disease (PD) in our previous studies using 2D APT imaging based on deep nuclei. We hypothesized that the pathophysiological abnormality of PD will change the APT-related parameters in the cerebral cortex, and the signal changes can contribute to accurate diagnosis of PD. METHODS: 34 patients with idiopathic Parkinson's disease (IPD) and 29 age- and sex-matched normal controls (NC) were enrolled in this prospective study. 3D-APT imaging and 3D-T1WI was performed in our participants. A volume-based morphometry algorithm was used and get automated cortical segmentations. Quantitative parameter maps of APT-related metrics were calculated by using SPM and MATLAB. The unpaired Student's t-test or Mann-Whitney U test was used for comparison of these values between IPD and NC groups. The associations between APT-related metrics and clinical assessments were investigated by Spearman correlation analysis. The receiver-operating characteristic (ROC) analysis was used to assess the diagnostic performances. The binary logistic regression model was used to combine the imaging parameters. RESULTS: There wasn't any correlations between cortical APT-related signals and clinical assessment, including the H&Y scale, the disease duration, the UPDRS III scores and the MMSE scores. The MTRasym, CESTRnr and MTRRex had significantly higher values (p <0.001, corrected by Bonferroni methods) in the IPD group than NC groups in the region of bilateral and total temporal grey matter. The single parameters achieved the best diagnostic performance among all APT-related metrics was MTRRex on the right temporal grey matter, with an area under the ROC curve (AUC) of 0.865. The combined parameters achieved the highest diagnostic performance (AUC: 0.932). CONCLUSIONS: 3D-APT imaging could identify the changes of the cerebral cortex in Parkinson's disease. The cortical changes of APT-related parameters could potentially serve as imaging biomarkers to aid in the non-invasive diagnosis of PD.

Microplastic biodegradability dependent responses of plastisphere antibiotic resistance to simulated freshwater-seawater shift in onshore marine aquaculture zones.

MPs carrying ARGs can travel between freshwater and seawater due to intensive land-sea interaction in onshore marine aquaculture zones (OMAZ). However, the response of ARGs in plastisphere with different biodegradability to freshwater-seawater shift is still unknown. In this study, ARG dynamics and associated microbiota on biodegradable poly (butyleneadipate-co-terephthalate) (PBAT) and non-biodegradable polyethylene terephthalate (PET) MPs were investigated through a simulated freshwater-seawater shift. The results exhibited that freshwater-seawater shift significantly influenced ARG abundance in plastisphere. The relative abundance of most studied ARGs decreased rapidly in plastisphere after they entered seawater from freshwater but increased on PBAT after MPs entered freshwater from seawater. Besides, the high relative abundance of multi-drug resistance (MDR) genes occurred in plastisphere, and the co-change between most ARGs and mobile genetic elements indicated the role of horizontal gene transfer on ARG regulation. Proteobacteria was dominant phylum in plastisphere and the dominant genera, such as Allorhizobium-Neorhizobium-Pararhizobium-Rhizobium, Afipia, Gemmobacter and Enhydrobacter, were significantly associated with qnrS, tet and MDR genes in plastisphere. Moreover, after MPs entered new water environment, the ARGs and microbiota genera in plastisphere changed significantly and tended to converge with those in receiving water. These results indicated that MP biodegradability and freshwater-seawater interaction influenced potential hosts and distributions of ARGs, of which biodegradable PBAT posed a high risk in ARG dissemination. This study would be helpful for understanding the impact of biodegradable MP pollution on spread of antibiotic resistance in OMAZ.

The Effects of Light Therapy for Depression in Dementia: A Systematic Review and Meta-Analysis.

BACKGROUND: Depression is one of the most common symptoms in patients with dementia. OBJECTIVE: This meta-analysis aimed to evaluate the effect of light therapy on depression associated with dementia by using a single scale. METHODS: Published studies based on the terms including "Dementia", "depression", and "Phototherapy" were searched. Web of Science, PubMed, Embase, CiNii, CNKI, Wanfang Database, and China Biology Medicine disc were adopted to collect randomized controlled studies or cross-controlled studies using the Cornell Scale for Depression in Dementia (CSDD) until February 2022. GRADE and Review Manager Version 5.4.1 were employed to assess the risk of bias. A meta-analysis was conducted by R 4.0.2 software based on the changes in CSDD scores. RESULTS: A total of 1,055 studies were retrieved from the databases, and six studies were included after screening. Some 406 people with dementia were included with an average age of over 80 years. Forest plot results showed that light intervention improved depression scores of dementia patients (MD = -2.59, 95% CI: -4.46 to -0.71), and light intensity less than 1,000 lux improved depression symptoms of dementia patients (MD = -2.76, 95% CI: -4.55 to -0.97). An intervention that lasted 8 to 12 weeks was the most effective (MD = -3.77, 95% CI: -6.93 to -0.60), and non-stable interventions such as ceiling LED lights exerted more positive effects (MD = -2.12, 95% CI: -3.38 to -0.85). CONCLUSION: The overall results of the meta-analysis suggested that light intervention can improve the depressive symptoms of older patients with dementia.