Using sustained vowels to identify patients with mild Parkinson's disease in a Chinese dataset.

Introduction: Parkinson's disease (PD) is the second most common neurodegenerative disease and affects millions of people. Accurate diagnosis and subsequent treatment in the early stages can slow down disease progression. However, making an accurate diagnosis of PD at an early stage is challenging. Previous studies have revealed that even for movement disorder specialists, it was difficult to differentiate patients with PD from healthy individuals until the average modified Hoehn-Yahr staging (mH&Y) reached 1.8. Recent researches have shown that dysarthria provides good indicators for computer-assisted diagnosis of patients with PD. However, few studies have focused on diagnosing patients with PD in the early stages, specifically those with mH&Y ≤ 1.5. Method: We used a machine learning algorithm to analyze voice features and developed diagnostic models for differentiating between healthy controls (HCs) and patients with PD, and for differentiating between HCs and patients with mild PD (mH&Y ≤ 1.5). The models were independently validated using separate datasets. Results: Our results demonstrate that, a remarkable diagnostic performance of the model in identifying patients with mild PD (mH&Y ≤ 1.5) and HCs, with area under the ROC curve 0.93 (95% CI: 0.851.00), accuracy 0.85, sensitivity 0.95, and specificity 0.75. Conclusion: The results of our study are helpful for screening PD in the early stages in the community and primary medical institutions where there is a lack of movement disorder specialists and special equipment.

Effect of blood pressure on mortality in patients with cognitive impairment: a prospective cohort study.

Background: Cognitive impairment is a prevalent condition that substantially elevates mortality rates among the elderly. The impact of hypertension on mortality in older adults with cognitive impairment is a subject of contention. This study aims to examine the influence of hypertension on both all-cause and CVD-specific mortality in elderly individuals experiencing cognitive impairment within a prospective cohort. Methods: This study encompassed 2,925 participants (weighted 53,086,905) aged 60 years or older from National Health and Nutrition Examination Survey (NHANES) spanning 2011-2014. Incidence of all-cause and CVD-specific mortality was ascertained through linkage with National Death Index records until 31 December 2019. Survival was performed employing the Kaplan-Meier method. Hazard ratios (HRs) were calculated via Cox proportional hazards regression models. Results: Over the follow-up period of up to 9.17 years [with a median (IQR) time to death of 6.58 years], equivalent to 18,731.56 (weighted 3.46 × 108) person-years, there were a total of 576 recorded deaths. Participants with CI exhibited a 1.96-fold higher risk of all-cause mortality (95% CI: 1.55-2.49; p < 0.01) and a 2.8-fold higher risk of CVD-specific mortality (95% CI: 1.83-4.29; p < 0.01) in comparison to participants without CI. Among participants with CI, concurrent hypertension comorbidity was linked to a 2.73-fold elevated risk of all-cause mortality (95% CI: 1.78-4.17; p < 0.01) and a 5.3-fold elevated risk of CVD-specific mortality (95% CI: 2.54-11.04; p < 0.01). Further stratified analyses revealed that the combined effects of hypertension and CI on all-cause and CVD-specific mortality were more pronounced in participants aged 60-69 years compared to those aged 70-80 years (p for interaction <0.01). The primary findings exhibited resilience across a series of sensitivity analyses. Conclusions: Participants with CI exhibited a markedly elevated risk of all-cause and CVD-specific mortality when coexisting with hypertension. Appropriate management of hypertension in patients with CI may be helpful in reducing the excess risk of death.

On-demand electrically controlled melatonin release from PEDOT/SNP composite improves quality of chronic neural recording.

Long-time and high-quality signal acquisition performance from implantable electrodes is the key to establish stable and efficient brain-computer interface (BCI) connections. The chronic performance of implantable electrodes is hindered by the inflammatory response of brain tissue. In order to solve the material limitation of biological interface electrodes, we designed sulfonated silica nanoparticles (SNPs) as the dopant of Poly (3,4-ethylenedioxythiophene) (PEDOT) to modify the implantable electrodes. In this work, melatonin (MT) loaded SNPs were incorporated in PEDOT via electrochemical deposition on nickel-chromium (Ni-Cr) alloy electrode and carbon nanotube (CNT) fiber electrodes, without affecting the acute neural signal recording capacity. After coating with PEDOT/SNP-MT, the charge storage capacity of both electrodes was significantly increased, and the electrochemical impedance at 1 kHz of the Ni-Cr alloy electrodes was significantly reduced, while that of the CNT electrodes was significantly increased. In addition, this study inspected the effect of electrically triggered MT release every other day on the quality and longevity of neural recording from implanted neural electrodes in rat hippocampus for 1 month. Both MT modified Ni-Cr alloy electrodes and CNT electrodes showed significantly higher spike amplitude after 26-day recording. Significantly, the histological studies showed that the number of astrocytes around the implanted Ni-Cr alloy electrodes was significantly reduced after MT release. These results demonstrate the potent outcome of PEDOT/SNP-MT treatment in improving the chronic neural recording quality possibly through its anti-inflammatory property.

A Conductive Bioengineered Cardiac Patch for Myocardial Infarction Treatment by Improving Tissue Electrical Integrity.

Conductive scaffolds are of great value for constructing functional myocardial tissues and promoting tissue reconstruction in the treatment of myocardial infarction (MI). Here, a novel scaffold composed of silk fibroin and polypyrrole (SP50) with a typical sponge-like porous structure and electrical conductivity similar to the native myocardium is developed. An electroactive engineered cardiac patch (SP50 ECP) with a certain thickness is constructed by applying electrical stimulation (ES) to the cardiomyocytes (CMs) on the scaffold. SP50 ECP can significantly express cardiac marker protein (α-actinin, Cx-43, and cTnT) and has better contractility and electrical coupling performance. Following in vivo transplantation, SP50 ECP shows a notable therapeutic effect in repairing infarcted myocardium. Not only can SP50 ECP effectively improves left ventricular remodeling and restore cardiac functions, such as ejection function (EF), but more importantly, improves the propagation of electrical pulses and promote the synchronous contraction of CMs in the scar area with normal myocardium, effectively reducing the susceptibility of MI rats to arrhythmias. In conclusion, this study demonstrates a facile approach to constructing electroactive ECPs based on porous conductive scaffolds and proves the therapeutic effects of ECPs in repairing the infarcted heart, which may represent a promising strategy for MI treatment.

ß-Hydroxybutyrate alleviates pyroptosis in MPP+/MPTP-induced Parkinson's disease models via inhibiting STAT3/NLRP3/GSDMD pathway.

BACKGROUND: Parkinson's disease (PD) is a common neurodegenerative disease characterized by motor symptoms and non-motor symptoms, and affects millions of people worldwide. Growing evidence implies ß-Hydroxybutyrate (BHB), one of the ketone bodies generated by ketogenesis, plays a neuroprotective role in neurodegenerative diseases. We aimed to verify the anti-inflammatory effect of BHB on PD and further explore potential molecular mechanisms. METHODS: We performed the experiments on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mice model in vivo and 1-methyl-4-phenylpyridinium (MPP+)-simulated BV2 cell model in vitro, with or without BHB pretreatment. Motor function was assessed by pole test, forced swimming test, traction test and open field test. Immunofluorescence was used to evaluate the loss of dopaminergic neurons and glial cell activation in MPTP-induced PD model mice. The expression of the STAT3/NLRP3/GSDMD signal pathway was measured by western blots. Proinflammatory cytokines was assessed by enzyme-linked immunosorbent assay (ELISA). RESULTS: BHB treatment reversed motor deficits, loss of dopaminergic neurons and glial cell activation in PD mice induced by MPTP. Moreover, BHB inhibited microglia pyroptosis by negatively regulating STAT3/NLRP3/GSDMD signal pathway, resulting in downregulation of proinflammatory cytokines (IL-1ß and IL-18) in vivo and vitro. CONCLUSION: These data suggested BHB supplement inhibited pyroptosis by down-regulating STAT3-mediated NLRP3 inflammasome activation for PD models in vivo and in vitro. Our findings provided novel insights and available interventions for the prevention and treatment of PD, and highlighted pyroptosis as a potential therapeutic target for PD.

Identification of Potential miRNA-mRNA Regulatory Network Contributing to Parkinson's Disease.

Parkinson's disease (PD) is a common neurodegenerative disease, and the mechanism underlying PD pathogenesis is not completely understood. Increasing evidence indicates that microRNAs (miRNAs) play a critical regulatory role in the pathogenesis of PD. This study aimed to explore the miRNA-mRNA regulatory network for PD. The differentially expressed miRNAs (DEmis) and genes (DEGs) between PD patients and healthy donors were screened from the miRNA dataset GSE16658 and mRNA dataset GSE100054 downloaded from the Gene Expression Omnibus (GEO) database. Target genes of the DEmis were selected when they were predicted by three or four online databases and overlapped with DEGs from GSE100054. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were then conducted by Database for Annotation, Visualization and Integrated Discovery (DAVID) and Metascape analytic tools. The correlation between the screened genes and PD was evaluated with the online tool Comparative Toxicogenomics Database (CTD), and protein-protein interaction (PPI) networks were built by the STRING platform. We further investigated the expression of genes in the miRNA-mRNA regulatory network in blood samples collected from PD patients and healthy donors via qRT-PCR. We identified 1505 upregulated and 1302 downregulated DEGs, and 77 upregulated and 112 downregulated DEmis were preliminarily screened from the GEO database. Further functional enrichment analysis identified 10 PD-related hub genes, including RAC1, IRS2, LEPR, PPARGC1A, CAMKK2, RAB10, RAB13, RAB27B, RAB11A, and JAK2, which were mainly involved in Rab protein signaling transduction, AMPK signaling pathway, and signaling by Leptin. A miRNA-mRNA regulatory network was then constructed with 10 hub genes, and their interacting miRNAs overlapped with DEmis, including miR-30e-5p, miR-142-3p, miR-101-3p, miR-32-3p, miR-508-5p, miR-642a-5p, miR-19a-3p, and miR-21-5p. Analysis of clinical samples verified significant upregulation of LEPR and downregulation of miR-101-3p and miR-30e-5p in PD patients as compared with healthy donors. Thus, the miRNA-mRNA regulatory network was initially constructed and has the potential to provide novel insights into the pathogenesis and treatment of PD.

Effects of Ketogenic Diet on Neuroinflammation in Neurodegenerative Diseases.

The ketogenic diet (KD) is a low-carbohydrate, high-fat and adequate-protein diet. As a diet mimicking fasting, it triggers the production of ketone bodies (KBs) and brings the body into a state of ketosis. Recent and accumulating studies on humans and animal models have shown that KD is beneficial to neurodegenerative diseases through modulating central and peripheral metabolism, mitochondrial function, inflammation, oxidative stress, autophagy, and the gut microbiome. Complicated interplay of metabolism, gut microbiome, and other mechanisms can regulate neuroinflammation in neurodegenerative diseases by activating multiple molecular and cellular pathways. In this review, we detail the physiological basis of the KD, its functions in regulating neuroinflammation, and its protective role in normal brain aging and neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD). We aimed to elucidate the underlying neuroinflammatory mechanisms of KD therapies in neurodegenerative diseases and provide novel insights into their application for neurodegenerative disease prevention and treatment.

Endogenous ceramide phosphoethanolamine modulates circadian rhythm via neural-glial coupling in Drosophila.

While endogenous lipids are known to exhibit rhythmic oscillations, less is known about how specific lipids modulate circadian behavior. Through a series of loss-of-function and gain-of-function experiments on ceramide phosphoethanolamine (CPE) synthase of Drosophila, we demonstrated that pan-glial-specific deficiency in membrane CPE, the structural analog of mammalian sphingomyelin (SM), leads to arrhythmic locomotor behavior and shortens lifespan, while the reverse is true for increasing CPE. Comparative proteomics uncovered dysregulated synaptic glutamate utilization and transport in CPE-deficient flies. An extensive genetic screen was conducted to verify the role of differentially expressed proteins in circadian regulation. Arrhythmic locomotion under cpes1 mutant background was rescued only by restoring endogenous CPE or SM through expressing their respective synthases. Our results underscore the essential role of CPE in maintaining synaptic glutamate homeostasis and modulating circadian behavior in Drosophila. The findings suggest that region-specific elevations of functional membrane lipids can benefit circadian regulation.

TMT-based quantitative proteome profiles reveal the memory function of a whole heart decellularized matrix for neural stem cell trans-differentiation into the cardiac lineage.

Whole organ or tissue decellularized matrices are a promising scaffold for tissue engineering because they maintain the specific memory of the original organ or tissue. A whole organ or tissue decellularized matrix contains extracellular matrix (ECM) components, and exhibits ultrastructural and mechanical properties, which could significantly regulate the fate of stem cells. To better understand the memory function of whole organ decellularized matrices, we constructed a heart decellularized matrix and seeded cross-embryonic layer stem cells - neural stem cells (NSCs) to repopulate the matrix, engineering cardiac tissue, in which a large number of NSCs differentiated into the neural lineage, but besides that, NSCs showed an obvious tendency of trans-differentiating into cardiac lineage cells. The results demonstrated that the whole heart decellularized microenvironment possesses memory function. To reveal the underlying mechanism, TMT-based quantitative proteomics analysis was used to identify the differently expressed proteins in the whole heart decellularized matrix compared with a brain decellularized matrix. 937 of the proteins changed over 1.5 fold, with 573 of the proteins downregulated and 374 of the proteins upregulated, among which integrin ligands in the ECM serve as key signals in regulating NSC fate. The findings here provide a novel insight into the memory function of tissue-specific microenvironments and pave the way for the therapeutic application of personalized tissues.

Dyskinesia-hyperpyrexia syndrome in Parkinson's disease: a systematic review.

PURPOSE: Dyskinesia-hyperpyrexia syndrome (DHS) is a rare but life-threatening disease. The clinical manifestations of this syndrome overlap substantially with Parkinson hyperpyrexia syndrome and serotonin syndrome and are often confused by clinicians. The purpose of this review was to enable clinicians to recognize this syndrome and thereby reach a correct diagnosis and provide optimal treatments to improve prognosis in clinical practice. METHODS: Using the methodology described in the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement, we conducted a literature search of the PubMed, Embase, and MEDLINE databases using keywords in titles and abstracts of published literature. Quality assessment was performed using the modified Newcastle-Ottawa scale. RESULTS: A total of 11 patients obtained from nine publications were included in this systematic review. All of the cases occurred in patients with advanced Parkinson's disease (PD) of long disease duration. High ambient temperature was the most common trigger of this syndrome. Hyperpyrexia and dyskinesias were present in all cases. The consciousness disturbances of this syndrome included confusion, hallucination, and lethargy or stupor. Autonomic dysfunction (except for hyperpyrexia) is uncommon in DHS, and only two patients presented with tachycardia. The treatment of this syndrome included supportive interventions (including rehydration, anti-pyretic and anti-infection treatments, and maintaining electrolyte balance), dopaminergic drug reduction and sedation. Two patients died due to DHS. CONCLUSIONS: We summarized the triggers, clinical features, and treatments of all reported dyskinesia-hyperpyrexia syndrome cases, proposed guiding diagnostic criteria, and established a flow chart to guide diagnoses to quickly identify these three syndromes in clinical practice.

Deep cerebral microbleeds are associated with the severity of lacunar infarcts and hypertension: A retrospective analysis.

Cerebral microbleeds (CMBs) and lacunar infarcts are common manifestations of cerebral small vessel disease. However, the association between the location of CMBs and lacunar infarcts is unclear. Our study aimed to clarify the relationship between the location of CMBs and lacunar infarcts.This study retrospectively analyzed 166 patients with ischemic stroke or transient ischemic attacks admitted in the Geriatric Neurology Department of Chinese PLA General Hospital between February 2010 and December 2012. We collected clinical characteristics and risk factors of CMBs. The location of CMBs on T2*-weighted angiography was assessed by the Microbleed Anatomical Rating Scale. The number of lacunar infarcts and the severity of white matter hyperintensities were also recorded. The association between the location of CMBs and lacunar infarcts parameters was examined.CMBs were present in 77 (46.4%) patients. The presence [odds ratios (OR), 2.14; 95% confidence interval (CI), 1.02-4.48], number (OR, 1.17; 95% CI, 1.02-1.36 per lesion), severity (OR, 1.61; 95% CI, 1.07-2.42) of lacunar infarcts, and hypertension (OR, 5.76; 95% CI, 2.01-16.55) were independent risk factors for CMBs. Stratified by the location of CMBs, lobar CMBs and infratentorial CMBs did not show significant association with lacunar infarcts. Deep CMBs were significantly associated with the number (OR 1.18, 95% CI 1.03-1.36) and severity (OR 1.71, 95% CI 1.11-2.63) of lacunar infarcts. Moreover, the percentage of deep CMBs increased with the increased severity of lacunar infarcts (P = .003).Deep CMBs rather than lobar and infratentorial CMBs are associated with lacunar infarcts.

Multi-modality molecular imaging characteristics of dementia with Lewy bodies.

Objective Dementia with Lewy bodies (DLB) is a common type of neurodegenerative dementia. Molecular neuroimaging using dopamine transporter (DaT), Pittsburgh compound B (PIB), and fluorodeoxyglucose (FDG) positron emission tomography (PET) has advantages in detecting dopaminergic neuron loss, abnormal amyloid ß-protein deposition, and glucose metabolism changes in patients with neurodegenerative disorders. However, the multi-modality molecular imaging features of patients with DLB have rarely been reported. Methods Five patients with a probable diagnosis of DLB were enrolled. PET/magnetic resonance imaging was performed with three tracers: 11C-ß-CFT, 11C-PIB, and 18F-FDG. Clinical and imaging characteristics were analyzed. Results All patients with DLB showed reduced uptake in the bilateral putamen on DaT PET, increased uptake throughout the cerebral cortex on PIB PET, and intact metabolism of the posterior cingulate gyrus on FDG PET. Conclusion Multimodal molecular imaging is helpful for early diagnosis of DLB. Studies with larger sample sizes are needed to confirm the molecular imaging differences between DLB and Alzheimer's disease and Parkinson's disease dementia.

A Presynaptic Function of Shank Protein in Drosophila.

Human genetic studies support that loss-of-function mutations in the SH3 domain and ankyrin repeat containing family proteins (SHANK1-3), the large synaptic scaffolding proteins enriched at the postsynaptic density of excitatory synapses, are causative for autism spectrum disorder and other neuropsychiatric disorders in humans. To better understand the in vivo functions of Shank and facilitate dissection of neuropathology associated with SHANK mutations in human, we generated multiple mutations in the Shank gene, the only member of the SHANK family in Drosophila melanogaster Both male and female Shank null mutants were fully viable and fertile with no apparent morphological or developmental defects. Expression analysis revealed apparent enrichment of Shank in the neuropils of the CNS. Specifically, Shank coexpressed with another PSD scaffold protein, Homer, in the calyx of mushroom bodies in the brain. Consistent with high expression in mushroom body calyces, Shank mutants show an abnormal calyx structure and reduced olfactory acuity. These morphological and functional phenotypes were fully rescued by pan-neuronal reexpression of Shank, and only partially rescued by presynaptic but no rescue by postsynaptic reexpression of Shank. Our findings thus establish a previously unappreciated presynaptic function of Shank.SIGNIFICANCE STATEMENT Mutations in SHANK family genes are causative for idiopathic autism spectrum disorder. To understand the neural function of Shank, a large scaffolding protein enriched at the postsynaptic densities, we examined the role of Drosophila Shank in synapse development at the peripheral neuromuscular junctions and the central mushroom body calyx. Our results demonstrate that, in addition to its conventional postsynaptic function, Shank also acts presynaptically in synapse development in the brain. This study offers novel insights into the synaptic role of Shank.

Gap junction networks in mushroom bodies participate in visual learning and memory in Drosophila.

Gap junctions are widely distributed in the brains across species and play essential roles in neural information processing. However, the role of gap junctions in insect cognition remains poorly understood. Using a flight simulator paradigm and genetic tools, we found that gap junctions are present in Drosophila Kenyon cells (KCs), the major neurons of the mushroom bodies (MBs), and showed that they play an important role in visual learning and memory. Using a dye coupling approach, we determined the distribution of gap junctions in KCs. Furthermore, we identified a single pair of MB output neurons (MBONs) that possess a gap junction connection to KCs, and provide strong evidence that this connection is also required for visual learning and memory. Together, our results reveal gap junction networks in KCs and the KC-MBON circuit, and bring new insight into the synaptic network underlying fly's visual learning and memory.

Cerebral microbleeds are associated with deep white matter hyperintensities, but only in hypertensive patients.

Cerebral microbleeds (CMBs) and white matter hyperintensities (WMH) are the most common manifestations of small vessel disease, and often co-occur in patients with cerebral vascular disease. Hypertension is widely accepted as a risk factor for both CMBs and WMH. However, the effect of hypertension on the association between CMBs and WMH remains unclear. We hypothesized that the relationship between CMBs and WMH is determined by hypertension. One hundred forty-eight patients with acute cerebrovascular disease who were admitted to PLA general hospital in Beijing, China from February 2010 to May 2011 were recruited in this study. CMBs on T2*-weighted angiography (SWAN) were assessed using the Brain Observer Microbleed Rating Scale criteria. The severity of the WMH was separately assessed as either peri-ventricular hyperintensities (PVH) or deep white matter hyperintensities (DWMH). The association among CMBs and the severity of WMH, and hypertension were determined. CMBs were found in 65 (43.9%) patients. The frequency of CMBs was related to the severity of DWMH and PVH. CMBs were more frequently observed in patients with hypertension compared to patients without hypertension (51.3% vs. 20.0%, p = 0.001). Hypertension was an independent risk factor for CMBs (odds ratio 5.239, p = 0.001) and DWMH (odds ratio 2.373, p = 0.040). Furthermore, the relationship between the presence of CMBs and the severity of DWMH was only found in patients with hypertension (r = 0.298, p<0.01). However, CMBs were associated with PVH independently of hypertension. This study demonstrated that hypertension determined the association between CMBs and DWMH.

Clinical features of dementia with lewy bodies in 35 Chinese patients.

OBJECTIVE: To investigate the clinical features of dementia with Lewy bodies (DLB) in a Chinese population. METHODS: Computer-based online searches through China Biology Medicine disc and China National Knowledge Infrastructure were performed to collect case reports of DLB published between 1980 and 2012. Clinical characteristics were analyzed. RESULTS: A total of 18 studies comprising 35 patients (26 males and 9 females) were included. The mean age at onset was 67.2 ± 9.8 years. Onset was characterized by memory impairment and accounted for 58.8% of all cases, followed by parkinsonism (11.8%), visual hallucinations (8.8%), and compulsive personality disorder (2.9%). The other patients (17.6%) presented two of the three core features of DLB at onset. With disease progression, parkinsonism was reported in 100% of cases, followed by visual hallucinations (97.1%), psychiatric symptoms (85.7%), severe neuroleptic sensitivity (81.8%), fluctuating cognition (68.6%), repeated falls (40.0%), sleep disorders (22.9%), and transient loss of consciousness (17.1%). 26 patients who were subjected to Mini-Mental State Examination scored ≤ 24. 10 patients presented relative preservation of hippocampus and medial temporal lobe structures on CT/MRI scan. Occipital hypometabolism occurred in 2 of 3 patients who underwent SPECT/PET perfusion scan. 12 patients showed an increasing of slow frequency activity on EEG, prominently in frontal and temporal lobes. CONCLUSIONS: DLB often strikes elderly individuals. Its clinical core features are dementia, fluctuating cognition, recurrent visual hallucinations and spontaneous features of parkinsonism. Neuropsychological, neuroimaging and EEG examinations may improve the diagnostic accuracy and discriminate DLB from other dementias.

[Application of A(2)DS(2) score for predicting post-stroke pneumonia in elderly patients].

OBJECTIVE: To investigate the risk factors for post-stroke pneumonia and assess the value of A(2)DS(2) score in predicting post-stroke pneumonia in elderly stroke patients. METHODS: The clinical data were retrospectively collected from elderly stroke patients from January, 2007 to December, 2012. A(2)DS(2) score was then assigned using the clinical information from the medical record. The ability of the score to discriminate between patients with post-stroke pneumonia and those without was quantified using ROC analysis. The calibration of the score was analyzed using Hosmer-Lemeshow goodness-of-fit test. RESULTS: A total of 131 elderly male stroke patients were enrolled in this study, among whom the incidence of post-stroke pneumonia was 29.01%. The independent risk factors for post-stroke pneumonia identified included moderate (P=0.0081, OR: 5.6089; 95%CI: 1.5663-20.0854) and severe (P=0.0048, OR: 44.4827; 95%CI: 3.1847-621.3126) neurological impairment, dysphagia (P=0.0005, OR: 7.5265; 95%CI: 2.4282-23.3292), and atrial fibrillation (P=0.0226, OR: 4.1778; 95%CI: 1.2221-14.2825). The incidence of post-stroke pneumonia ranged from 2.2% in patients with a A(2)DS(2) score less than 3 to 75% in those with a score higher than 8. The C-statistic of A(2)DS(2) score for predicting post-stroke pneumonia was 0.86 (95%CI: 0.784-0.911) by the ROC analysis. The A(2)DS(2) score was well calibrated to predict post-stroke pneumonia in elderly patients by Hosmer-Lemeshow test (7.083, P=0.528). CONCLUSION: The A(2)DS(2) score can be useful for predicting post-stroke pneumonia and for routine monitoring of high-risk elderly stroke patients in the clinical setting.

[Neuropsychological features of elderly patients with mild cognitive impairment susceptible to Alzheimer's disease].

OBJECTIVE: To explore the neuropsychological features of elderly patients with mild cognitive impairment (MCI) susceptible to Alzheimer's disease (AD). METHODS: A total of 47 patients with MCI diagnosed from June to October 2008 and 21 controls with normal cognition at the same convalescent camp were selected and followed up for two years. Montreal cognitive assessment (MoCA), mini mental state examination (MMSE) and clock drawing test (CDT) were performed for all subjects at the onset of study and repeated annually. RESULTS: At Month 12, the visuospatial skill scores of MCI patients decreased significantly versus those of the control (0.6 ± 0.7 vs 0.1 ± 0.6, P = 0.008). No one progressed to AD in neither groups. And at Month 24, both visuospatial skill scores (0.9 ± 0.9 vs 0.4 ± 0.9) and attention scores (1.0 ± 1.0 vs 0.2 ± 0.8) of MCI patients declined significantly versus the control (P = 0.021, 0.001). Among 47 MCI patients, 7 progressed to AD. No obvious difference existed in the score of all items between the AD converters and non-converters at baseline. However, the scores of MMSE (27.6 ± 0.8 vs 28.9 ± 1.0), MoCA (24.3 ± 3.1 vs 27.9 ± 1.6) and such MoCA subitems as visuospatial skill (3.9 ± 0.7 vs 4.5 ± 0.6), language (1.86 ± 0.38 vs 2.65 ± 0.53) and delayed recall (2.1 ± 1.5 vs 3.9 ± 1.0) of the converters were obviously lower than those of the non-converters at Month 12 (P < 0.05). Furthermore, all other scores of the AD converters, except for designation and abstract, were significantly lower than those of the non-converters at Month 24 (P < 0.05). CONCLUSION: The visuospatial skill, executive function, delayed recall and language function of MCI patients progressing to AD tend to have early impairment and significant changes. It may be useful to predict AD among the MCI patients.

[A follow-up study on cognitive changes of mild cognitive impairment in the elderly].

OBJECTIVE: To observe and assess the cognitive changes of mild cognitive impairment (MCI) in the elderly. METHODS: A cohort study design was conducted among 47 patients with MCI and 21 control selected from the same convalescent camp, Montreal cognitive assessment (MoCA), mini mental state examination (MMSE) and clock drawing test (CDT) were performed to all subjects at the onset of study and 12 months later. RESULTS: The score of MMSE, CDT, MoCA and its subitems including visuospatial skill and delayed recall of MCI group were lower than the baseline after 12 months, with significantly decline in the score of MoCA (P = 0.041) and delay recall (P = 0.003). There was no obvious difference in the score of control between the baseline and that after 12 months. CONCLUSION: The decline of delayed recall occurred early and significantly, which may be a predictor in the conversion of mild cognitive impairment to dementia.

[A cross-sectional study of neurological disease in the veterans of military communities in Beijing].

OBJECTIVE: To investigate the prevalence of cognitive and motor disorders as well as emotional and sleep abnormality in the veterans from military communities in Beijing. METHODS: The participants underwent a comprehensive in-person evaluation including detailed neuropsychological testing, Hospital Anxiety and Depression Scale and special questionnaires for movement and sleep disorders. RESULTS: The overall prevalence of cognitive impairment, extrapyramidal diseases was 32.7%, 8.8%. The prevalence of mild cognitive impairment, dementia, Parkinson disease, essential tremor, anxiety and depression was 26.2%, 6.5%, 2.0%, 6.1%, 1.4% and 4.1% respectively. Prevalence of all kinds of sleep disorders ranged from 10.3% to 53.9%. The prevalence of cognitive impairment had no significant difference of sex, but were correlated to age and education, the correlation coefficient was 0.326 and -0.221 (P<0.01). CONCLUSION: Veterans from military communities had higher prevalence of cognitive impairment, extrapyramidal diseases and sleep disorders and lower that of anxiety and depression relatively.