Myasthenia gravis is generally regarded as an autoantibody-mediated autoimmune disease, while whether myogenic factors trigger this immune disorder remains elusive. Our previous studies identified carbonic anhydrase 3 (CAR3) that is significantly downregulated in muscles from myasthenia gravis patients and plays an essential role in myasthenia gravis pathogenesis. In the present study, using experimental autoimmune myasthenia gravis (EAMG) mouse model generated with muscle specific Car3 deficient (Acta1creCar3f/f) mice, we found that Car3 deficiency in muscle considerably exacerbated myasthenia symptoms. Importantly, EAMG Acta1creCar3f/f mice exhibited substantial T follicular helper (TFH) differentiation in muscle and significantly elevated levels of anti-AChR autoantibodies. Additionally, we detected increased intracellular complement C3a in Car3 deficient muscle cells. RNA-seq analysis and genetic validation experiments illustrated that Car3 deficiency facilitates intracellular C3a production via cathepsin S. Once released, myogenic C3a binds to C3a receptor on T cells, thereby driving TFH differentiation and subsequent autoantibody production. Collectively, our results demonstrate that Car3 deficiency promotes intracellular C3 activation in muscle cells and induces TFH differentiation, revealing a critical role of muscle-immune communication in the pathogenesis of myasthenia gravis.

Myocardial ischemia/reperfusion (I/R) injury undermines the clinical benefit of percutaneous coronary intervention, with cardiac macrophages playing critical roles. Here, using spatial transcriptomics and flow cytometry, we identified adenylyl cyclase 7 (ADCY7) as a macrophage-specific regulator and potential therapeutic target in myocardial I/R injury, and validated its expression in patient samples. By establishing a macrophage depletion/reconstitution model, we demonstrate that macrophage Adcy7 deficiency significantly exacerbates myocardial I/R injury and cardiac dysfunction in male mice, whereas Adcy7 overexpression attenuates these effects. Macrophage Adcy7 deficiency also increases leukocyte infiltration and pro-inflammatory cytokine production. Mechanistically, transcriptomic and phosphoproteomic analyses reveal that ADCY7 activates cAMP-protein kinase A signaling, thereby inhibiting nuclear translocation of NF-κB and restraining the pro-inflammatory response. Combined with the macrophage depletion/reconstitution approach, we developed a photoactivated adenylyl cyclase system that alleviated cardiac inflammation and I/R injury. Our study identifies ADCY7 as a macrophage-intrinsic anti-inflammatory regulator and a promising therapeutic target for myocardial I/R injury.

BackgroundIn cerebral small vessel disease (CSVD), the burden of white matter hyperintensities (WMH) does not fully account for cognitive impairment, suggesting the involvement of intermediary mechanisms.ObjectiveWe investigated whether a gray matter atrophy network acts as the key mediator linking topologically specific (deep) WMH to multidomain cognitive dysfunction.MethodsIn this retrospective study, 260 patients with CSVD (62 cognitively normal, 125 with mild impairment, 73 with dementia) were included. Cognitive status was assessed neuropsychologically. 3.0 T MRI identified an atrophy network. We then conducted pre-specified mediation analyses and a primary confirmatory analysis using structural equation modeling (SEM) to test whether this atrophy network mediated the effect of deep WMH on cognitive performance.ResultsA 41-region atrophy network was identified, primarily involving the medial temporal lobe and thalamus, that was significantly associated with cognitive status. The final SEM demonstrated excellent fit, showing that higher deep WMH burden was associated with greater network atrophy (β = 0.145, p < 0.05), which in turn was strongly associated with poorer executive function (β = -0.64, p < 0.001) and memory (β = -0.572, p < 0.001). The direct effect of WMH on cognition was not statistically significant in the model.ConclusionsOur findings suggest that in CSVD, a unified network of gray matter atrophy acts as a powerful statistical mediator in the effect of deep white matter injury on cognitive decline. This atrophy pattern may represent a more direct biomarker of the neurodegenerative process underlying cognitive impairment than WMH burden alone.

Accelerated CHRN/AChR/nicotinic acetylcholine receptor internalization induced by auto-antibodies impairs neuromuscular junction transmission and contributes to myasthenia gravis (MG), a typical autoimmune disease. Although CHRN internalization is well established in MG pathogenesis, the downstream cellular events, especially those related to autophagy, remain poorly described. Here, we report that RAPSN/rapsyn, an intracellular CHRN-binding protein essential for its clustering, accumulates as aggregates in experimental autoimmune myasthenia gravis (EAMG) mice. In CHRN antibody-treated myotubes, RAPSN dissociates from internalized CHRN and forms aggregates due to exposure of its hydrophobic domains. These aggregates in turn impair the trafficking and membrane incorporation of newly synthesized CHRN, thereby exacerbating CHRN loss. Notably, the accumulation of RAPSN aggregates facilitates formation of HSPA/HSP70-BAG3 complex, which recognizes and transports the aggregates along microtubules to form perinuclear aggresomes for subsequent lysosomal degradation. Accordingly, pharmacological inhibition or knockdown of HSPA-BAG3 complex increases RAPSN aggregation, which participates in enhanced CHRN loss and worsened muscle weakness in EAMG mice. This study identifies HSPA-BAG3 aggrephagy as a protective mechanism that clears RAPSN aggregates to maintain CHRN integrity and suggests a potential therapeutic strategy for MG.Abbreviation: 3-MA: 3-methyladenine; AAV: adeno-associated virus; CASA: chaperone-assisted selective autophagy; CHRN/nicotinic acetylcholine receptor: cholinergic receptor nicotinic; CHRN-ab: CHRN antibodies; CHX: cycloheximide; CMAP: compound muscle action potential; CQ: chloroquine; EAMG: experimental autoimmune myasthenia gravis; ER: endoplasmic reticulum; GAS: gastrocnemius; MAP1LC3A/B: microtubule associated protein 1 light chain 3 alpha/beta; MG: myasthenia gravis; NMJ: neuromuscular junction; Rapa: rapamycin; RAPSN/rapsyn: receptor associated protein of the synapse; SQSTM1: sequestosome 1; TA: tibialis anterior; αBTX-A594: α-bungarotoxin-Alexa-594.

BACKGROUND:Sepsis-associated encephalopathy (SAE) is characterised by cognitive impairment and is a common complication in patients with sepsis. Microglia are involved in various cognitive impairment-related diseases through phagocytic synapses. Cholecystokinin (CCK), an abundant neuropeptide in the brain, is closely related to cognitive function. However, the role of CCK in SAE and the relationship between CCK and microglial phagocytosis of synapses are unknown. METHODS:Lipopolysaccharide (LPS) was used to construct SAE models in 3-month-old male mice and BV2 microglial cells. To investigate the effects of CCK on cognitive impairment in SAE model mice, we used exogenous CCK injection into the dorsal hippocampal CA1 region or the chemogenetic activation of CCK-positive neurons to promote endogenous CCK release. Morris water maze and fear conditioning test were used to assess cognitive function in mice. RNA sequencing was performed to explore the potential signalling pathways involved in CCK-induced neuroprotection. Western blot and immunofluorescence were used to assess the effects of CCK on microglial phagocytosis of synapses, neurotoxic astrocytes, and excitatory synapses. Whole-cell recording was used to determine excitatory synaptic transmission. RESULTS:LPS successfully established in vivo and in vitro models of SAE. Both exogenous CCK injection and activation of CCK-positive neurons in hippocampal CA1 region attenuated cognitive impairment in SAE mice. Mechanistically, CCK significantly alleviated excitatory synaptic plasticity damage via inhibiting complement 1q (C1q)-mediated microglial phagocytosis of synapses and neurotoxic astrocyte polarisation. Moreover, in vitro SAE model of BV2 cells demonstrated that CCK exerts neuroprotective effects through microglial CCK2-type receptor. CONCLUSIONS:CCK may alleviate cognitive impairment by inhibiting microglia C1q-mediated phagocytosis of excitatory synapses, suggesting that both CCK drugs and specific activation of CCK-positive neurons are potential treatments for SAE.

Skeletal muscle function gradually declines with aging, presenting substantial health and societal challenges. Comparative analysis of how aging affects fast- and slow-twitch muscles remains lacking. We utilized 20-month-old mice to reveal the aging effects on muscle structure and fiber composition, followed by bulk RNA sequencing for fast- and slow-twitch muscles and integration with human single-cell RNA sequencing dataset providing a comparative analysis across species. In mouse slow-twitch muscles, aging induced a switch from fast to slow fibers and distinctively altered lipid metabolism in ceramide and triglyceride, with the upregulation of regulatory genes Gk and Ppargc1a also observed in human slow fibers. Additionally, both types of muscles exhibited common collagen deposition and fibrosis, possibly due to the imbalance between collagen synthesis and degradation. The extracellular matrix gene changes substantially overlapped between mice and humans in aging, yet also highlighted clear differences. This integrative analysis provides further understanding of aged fast- and slow-twitch muscles and offers new insights into the molecular changes in aging.

Myasthenia gravis (MG) is an autoimmune disease that impairs neuromuscular transmission. Autoantibodies and cellular immunity mediate the immunopathology of MG, yet the mechanism of CD8+ T cells in this process remains elucidated. In this study, we discovered a novel subset of CD8αα+ T cells in the peripheral blood of an 18-year-old Chinese man diagnosed as MG, who has undergone thymectomy and persistent myasthenia crisis. Designated as CD161neg T cell, this subset was characterized by TCRαβ+CD8αα+PLZF+Vα7.2+ but notably lacked CD161, distinct from mucosal-associated invariant T (MAIT) cells known for high CD161. The patient exhibited unusually high levels of CD161neg T cells compared to other MG patients, which fluctuated with infections but not MG severity. RNA sequencing revealed that CD161neg T cells lacked the genes characteristic of mature MAIT cells including CCR6, CXCR6, ZBTB16, and IL18RAP, but expressed cytotoxic T cell-related genes GZMH and IFNG. This study shed new light on the heterogeneity and complexity of CD8αα+ T cells in MG patients with thymoma.

BACKGROUND:Little is known about the dynamic process of the outer-wall boundary during intensive lipid-lowering therapy in patients with intracranial atherosclerotic stenosis and its clinical implications. METHODS:We analyzed patients with first-ever acute ischemic stroke attributed to intracranial atherosclerotic stenosis who received intensive lipid-lowering therapy with high-dose statins or PCSK9i (proprotein convertase subtilisin/kexin type 9 inhibitor). Data were obtained from a multicenter cohort study at 15 hospitals across China and our institutional database in Beijing, China. All patients underwent 3-dimensional T1-weighted high-resolution magnetic resonance vessel wall imaging at baseline and after a >6-month follow-up period. Outer-wall boundary area changes were classified as expansion (>10% increase), shrinkage (>10% decrease), or quiescence (≤10% change). The association between these changes and time to recurrent ipsilateral stroke was assessed. The Kaplan-Meier method and the Cox proportional hazards model were used. RESULTS:Among the 137 patients, 50 (36.5%) exhibited expansion, 40 (29.2%) shrinkage, and 47 (34.3%) quiescence of the outer-wall boundary area. Among these 3 groups, plaque burden decreased significantly between the index imaging and follow-up (all P≤0.02). Lumen area increased significantly in patients with expansion (P<0.001) and quiescence (P=0.01) but not in those with shrinkage of the outer-wall boundary area (P=0.34). Patients with shrinkage of the outer-wall boundary area had a significantly increased risk of recurrent ipsilateral stroke (hazard ratio, 2.95 [95% CI, 1.02-8.55]; P=0.046) compared with patients without such shrinkage. In multivariable Cox regression analysis, shrinkage of the outer-wall boundary area was associated with recurrent ipsilateral stroke compared with non-shrinkage after adjusting for potential confounders (hazard ratio, 4.21 [95% CI, 1.14-15.58]; P=0.031). CONCLUSIONS:Outer-wall boundary area changes vary among patients with intracranial atherosclerotic stenosis under intensive lipid-lowering therapy. Shrinkage of the outer-wall boundary area is significantly associated with a higher risk of stroke recurrence.

Integrating dietary interventions have been extensively studied for their health benefits, such as Alzheimer's disease, Huntington's disease, and aging. However, it is necessary to fully understand the mechanisms of long-term effects and practical applications of these dietary interventions for health. A 10-week intermittent fasting (IMF) regimen was implemented on the aging animals in the current study. The variations of cerebral functions were analyzed employing a comprehensive experimental design that includes behavioral tests, neuroimaging, and ultrastructural analysis, such as resting-state functional MRI (rsfMRI), EEG/EMG recordings, transmission electron microscopy, and immunohistochemistry. Over a 10-week regimen, IMF significantly improved locomotor activity, motor coordination, and muscle strength compared to controls (p < 0.01). Resting-state fMRI (rsfMRI) demonstrated that IMF modulates brain-wide functional connectivity, enhancing communication between key brain regions. Advanced imaging techniques revealed increased expression of myelin-related proteins, including myelin basic protein (MBP), and myelin-associated glycoprotein (MAG), indicating enhanced myelin integrity and repair, particularly in axons with diameters < 400 nm (p < 0.01). These findings suggest that IMF may mitigate age-related declines by promoting better neuronal signaling. This study highlights the potential function of IMF as a non-pharmacological intervention to promote brain health and mitigate cognitive decline in aging populations.

Background and Objectives: This study aimed to investigate the association between high-resolution magnetic resonance imaging (HR-MRI) characteristics and recurrent ipsilateral stroke in patients with symptomatic intracranial atherosclerotic steno-occlusive disease (ICAS). Methods: This multicenter, observational study recruited first-ever acute ischemic stroke patients attributed to ICAS (>50% stenosis or occlusion) within 7 days after onset. Participants were assessed by multi-parametric MRI including diffusion-weighted imaging, three-dimension time-of-flight magnetic resonance angiography, and three-dimensional T1-weighted HR-MRI. The patients were recommended to receive best medical therapy and were systematically followed up for 12 months. The association between HR-MRI characteristics and the time to recurrent ipsilateral stroke was investigated by univariable and multivariable analysis. Results: Two hundred and fifty-five consecutive patients were enrolled from 15 centers. The cumulative 12-month ipsilateral recurrence incidence was 4.1% (95% confidence interval [CI]: 1.6-6.6%). The plaque length (5.69±2.21 mm vs. 6.67±4.16 mm), plaque burden (78.40±7.37% vs. 78.22±8.32%), degree of stenosis (60.25±18.95% vs. 67.50±22.09%) and remodeling index (1.07±0.27 vs. 1.03±0.35) on HR-MRI did not exhibit discernible difference between patients with and without recurrent ipsilateral stroke. Patients with recurrent ipsilateral stroke exhibited higher rates of intraplaque hemorrhage (IPH) (30.0% vs. 6.5%) and eccentric plaque (90.0% vs. 48.2%), and lower occurrence of occlusive thrombus (10.0% vs. 23.7%). In the multivariable Cox regression analysis, IPH (hazard ratio: 7.05, 95% CI: 1.53-32.41, p=0.012) was significantly associated with recurrent ipsilateral stroke after adjustment. Discussion: We found IPH is significantly associated with recurrent ipsilateral stroke. Our results suggest IPH has potential value in the selection of patients for aggressive treatment strategies.

BackgroundA high-fat diet (HFD) contributes to various metabolic disorders and obesity, which are major contributors to cardiovascular disease. As an essential regulator for heart homeostasis, cardiac resident macrophages may go awry and contribute to cardiac pathophysiology upon HFD. Thus, to better understand how HFD induced cardiac dysfunction, this study intends to explore the transcriptional and functional changes in cardiac resident macrophages of HFD mice.MethodsC57BL/6J female mice that were 6 weeks old were fed with HFD or normal chow diet (NCD) for 16 weeks. After an evaluation of cardiac functions by echocardiography, mouse hearts were harvested and cardiac resident CCR2- macrophages were sorted, followed by Smart sequencing. Bioinformatics analysis including GO, KEGG, and GSEA analyses were employed to elucidate transcriptional and functional changes.ResultsHyperlipidemia and obesity were observed easily upon HFD. The mouse hearts also displayed more severe fibrosis and diastolic dysfunction in HFD mice. Smart sequencing and functional analysis revealed metabolic dysfunctions, especially lipid-related genes and pathways. Besides this, antigen-presentation-related gene such as Ctsf and inflammation, particularly for NF-κB signaling and complement cascades, underwent drastic changes in cardiac resident macrophages. GO cellular compartment analysis was also performed and showed specific organelle enrichment trends of the involved genes.ConclusionDysregulated metabolism intertwines with inflammation in cardiac resident macrophages upon HFD feeding in mice, and further research on crosstalk among organelles could shed more light on potential mechanisms.

Objective: Serum metabolites from 19 myasthenia gravis (MG) patients and 15 normal controls were analyzed via untargeted metabolomics, including 6 pre/post-treatment paired MG patients, to assess the value of serum metabolites as biomarkers in monitoring MG. Method: Differential metabolites between MG patients and normal controls were identified through liquid and gas chromatography-mass spectrometry simultaneously. Principal component analysis and orthogonal partial least squares-discriminant analysis were conducted to identify the differential metabolites. Candidate metabolites and pathways associated with MG were selected through a random forest machine learning model. Result: A total of 310 differential metabolites were identified with a threshold of variable projected importance > 1 and P value < 0.05. Among these, 158 metabolites were upregulated and 152 were downregulated. The random forest machine learning model selected 5 metabolites as potential biomarkers associated with MG: lignoceric acid (AUC=0.944), uridine diphosphate-N-acetylglucosamine (AUC=0.951), arachidonic acid (AUC=0.951), beta-glycerophosphoric acid (AUC=0.933), and L-Asparagine (AUC=0.877). Further analysis using 6 paired MG patients pre- and post-immunosuppression treatment revealed 25 upregulated and 6 downregulated metabolites in post-treatment serum, which might be relevant to disease intervention. The significance remains elusive due to the limited number of patients. Conclusion: A subset of differential metabolites was identified in the serum of MG patients, some of which changed with immunosuppressive therapy. Small molecule metabolites may serve as valuable biomarkers for disease monitoring in MG.

Cardiovascular diseases are an array of age-related disorders, and accumulating evidence suggests a link between cardiac resident macrophages (CRMs) and the age-related disorders. However, how does CRMs alter with aging remains elusive. In the present study, aged mice (20 months old) have been employed to check for their cardiac structural and functional alterations, and the changes in the proportion of CRM subsets as well, followed by sorting of CRMs, including C-C Motif Chemokine Receptor 2 (CCR2)+ and CCR2– CRMs, which were subjected to Smart-Seq. Integrated analysis of the Smart-Seq data with three publicly available single-cell RNA-seq datasets revealed that inflammatory genes were drastic upregulated for both CCR2+ and CCR2– CRMs with aging, but genes germane to wound healing were downregulated for CCR2– CRMs, suggesting the differential functions of these two subsets. More importantly, inflammatory genes involved in damage sensing, complement cascades, and phagocytosis were largely upregulated in CCR2– CRMs, implying the imbalance of inflammatory response upon aging. Our work provides a comprehensive framework and transcriptional resource for assessing the impact of aging on CRMs with a potential for further understanding cardiac aging.

We reported four patients with coronavirus disease 2019 (COVID-19)–associated myelopathies, highlighting the delayed and atypical spinal cord magnetic resonance imaging (MRI) features and the literature review. All four patients were males, aged 37 to 72 years old. The latencies from COVID-19 to the onset of myelitis were 5, 15, 30, and 80 days. The initial symptoms were numbness and weakness of lower limbs in three cases, and back pain with weakness of lower limbs in one case. The peak symptoms included paraplegia, sphincter dysfunction, sensory disturbance level, and spastic gait. The EDSS scores were 7.5, 9.0, 9.0, and 7.5, respectively. Magnetic resonance imaging (MRI) showed delayed atypical spinal cord lesions at onset, i.e., two cases without lesions, one with linear spinal meningeal enhancement, and one with punctate lesions on T2-weighted imaging (T2WI). During the follow-up period, punctate, linear, and cloudy lesions in the lateral and posterior funiculus were seen on T2WI in the peak stage. The prominent features of spinal cord lesions were linear spinal meningeal enhancement, the mismatch of deteriorated clinical symptoms, and inapparent MRI findings. All four patients were left with an obvious disability, with two patients completely bedridden and two who could stand with support. This report highlights the recognition of COVID-19-associated myelopathy even months after initial infection, especially in patients with delayed and atypical spinal cord findings on MRI.

免疫耐受是机体对特定抗原不产生应答或产生低水平应答的状态，防止自身免疫性疾病的发生。自噬是溶酶体参与的细胞内分解代谢过程，对于免疫耐受的调节是不可或缺的，在淋巴细胞的阴性选择、诱导克隆无能和调节性T细胞的产生中均发挥重要的作用。自噬紊乱会引发多种自身免疫性疾病，如重症肌无力、克罗恩病和系统性红斑狼疮。该文主要对自噬的分子机制、中枢和外周耐受的自噬调节以及自噬在自身免疫性疾病发生发展中的作用进行综述，加深了对自噬在免疫耐受中作用的认识，为自身免疫性疾病的防治提供新靶点。

Background The increasing prevalence of Alzheimer’s disease (AD) has emerged as a major challenge worldwide. China as the most populous country in the globe is amid rapid aging of its population, highlighting the need for appropriate social and medical policies to meet the challenge. The current multicenter cross-sectional observational study aims to provide understanding of the current status of caring given to AD patients in China and investigate the factors that influence the family burden as well as the choice of care given to AD patients. Methods A total of 1,675 patients with probable AD from 30 provincial regions of mainland China were enrolled in the current study from August 2019 to December 2019. We analyzed the caregiving status and its relationship with family burden and various socio-economical and medical factors. Results In the current study, 90.87% of the AD patients enrolled adopted family care. The choice of caregiving method was influenced by factors including age (>80 years old, OR 0.648; 95% CI, 0.427–0.983), overall family burden (high, OR 0.574; 95% CI, 0.0.373–0.884), patients’ income (OR 0.511; 95% CI, 0.330–0.789) and self-care ability (OR 0.329; 95% CI, 0.183–0.588). Conclusion Family care is the primary method of care for AD patients in China and the institutional care system for AD patients is still underprepared in China.

Introduction In China, the increasing number of people with Alzheimer's disease (AD) poses a great challenge to families and the country. Economic and cultural differences cause a urban-rural gap in medical resources. This multicenter survey aimed to investigate the real-world practice of disease treatment among people with AD. Methods People with AD and their caregivers from 30 provincial regions in mainland China were enrolled from October 2020 to December 2020 to be surveyed for their treatment experience. Logistic regression was used to explore the factors that influence medication adherence in all areas, urban areas, and rural areas. Results In this survey, 1,427 participants came from urban areas, and 539 participants came from rural areas. Patients in urban areas were older (mean age 74 vs. 70, p = 0.001), less frequently had mild AD (36.0 vs. 52.1%, p < 0.001), and more often were cared for at professional institutions (8.8 vs. 3.2%, p < 0.001). In terms of pharmacotherapy, 77.8% of people accepted taking lifelong medication, whereas 61.3% of patients insisted on taking medications. Although 72.0% of rural people believed in taking lifelong medication, only 30.0% adhered to drug use. The major factors that influenced medication adherence for all patients with AD were regional distribution (p < 0.001, OR = 6.18, 95% CI: 4.93–7.74) and family earnings (p = 0.003, OR = 1.22, 95% CI: 1.07–1.38). In rural areas, family earnings (p = 0.008, OR = 1.44, 95% CI: 1.10–1.89) and severity of AD (p = 0.033, OR = 1.31, 95% CI: 1.02–1.68) were the main factors. Family earnings (p = 0.038, OR = 1.16, 95% CI: 1.01–1.34) was the only factor among urban areas. Among all non-pharmaceutical activities except for cognitive intervention, the participation rates of rural patients were significantly higher than those of urban patients (p < 0.05). Conclusion Although national progress has been made in the public awareness of disease treatment, adequate diagnosis and medication adherence need to be prompted, especially in rural areas. Furthermore, lifelong treatment should be improved based on regional characteristics through the joint efforts of the government, health workers, and social volunteers.

15q11.2 BP1-BP2 microdeletion is related to clinical abnormalities including general developmental delay, speech and neuropsychiatric disorders, which is known as Angelman syndrome. However, the clinical penetrance and phenotype of 15q11.2 BP1-BP2 deletion is varied and confusing. Herein, we retrospectively described a 50-year-old male patient who manifested with progressive spastic paraplegia of lower limbs and episodic exacerbation. While brain MRI showed white matter hyperintensities, lacunes, cerebral microbleeds, enlarged perivascular spaces, and brain atrophy, mimicking small vessel disease. Next-generation sequencing combining multiplex ligation-dependent probe amplification identified a 253 kb 15q11.2 BP1-BP2 microdeletion, encompassing 4 conserved imprinted genes (NIPA1, NIPA2, CYFIP1 and TUBGCP5). This report will build new connections among spastic paraplegia, small vessel disease and 15q11.2 BP1-BP2 microdeletion.

Background The prevalence of Alzheimer's disease (AD) is rapidly in China, which puts a great deal of pressure on the patient’s family and society. The way of patient care deserves social attention. This study focused on the caregiving status and the relationship between caregivers’ burden and patient factors based on the Chinese pension system. Methods This is a large-scale, multicenter cross-sectional study aimed to investigate the two types of caregiving (family care and nursing care), and the caregiver burden of patients with AD. A total of 1675 patients with a definite diagnosis of probable AD from 30 provincial, municipal, and autonomous regions of mainland China were enrolled from August 2019 to December 2019. Caregivers of AD patients completed the questionnaire under the guidance of trained investigators. The characteristics of patients and caregivers were summarized by descriptive statistics. Results Among the 1675 AD patients, 1522 (90.87%) patients adopted family care. There was a significant correlation between the housing condition, annual income, self-care ability, and the choice of caregiving (P < 0.05). According to the caregiver burden inventory score, 28.90% of the caregivers had a low burden, 57.01% had a medium burden and 14.09% had a heavy burden, concerning the patient's age, caring style, self-care ability, etc. The burden of the caregivers in the nursing facilities is relatively high than that of family care (P < 0.05). Conclusion Family care is the main way of care for AD patients in China. Caregiving status is affected by living place, patient income and severity of the disease. The burden of family caregivers of AD is generally high, especially patients with disabilities.