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Lu-ning Wang

Publications and source records attributed to Lu-ning Wang.

16 recordsLinked to original sources
PubMed2006

[A case-control study of risk factors in mild cognitive impairment].

OBJECTIVE: To explore the risk factors of mild cognitive impairment (MCI). METHODS: A case-control study including 97 MCI patients and 143 cognitive normal controls (NC) in Chinese PLA General Hospital was conducted. The cases and controls were matched for age, gender and occupation. The relationship between MCI and various factors was analysed by univariate and multivariate analysis. RESULTS: Results data from univariate analysis showed that the history of coronary heart diseases, stroke, anaemia, and the education level had significant differences between NC and MCI patients. Multivariate analysis confirmed that the history of coronary heart diseases, stroke, anaemia and the education level were significantly related to MCI and their ORs (95% confidence interval) were 2.21 (1.18 - 4.14), 2.18 (1.20 - 3.98), 4.63 (1.79 - 11.97), 0.75 (0.58 - 0.97) respectively. CONCLUSION: The history of coronary heart diseases, stroke and anaemia were independent risk factors of MCI and high education level seemed to be a protective factor of MCI.

Anemia↗
PubMed2006

[A nimodipine interventional study of patients with mild cognitive impairment].

OBJECTIVE: To observe the effect of nimodipine on the cognition status and the changes of metabolites in brain tissue in the patients with mild cognitive impairment (MCI) in order to evaluate the significance of intervening MCI with medication. METHODS: 31 patients with MCI were selected 16 cases were in a treatment group taking nimodipine for 3 months besides taking basic internal medication and 15 cases in a control group taking only basic internal medication. Before and after treatment, multiple cognition tests were carried out in both groups and magnetic resonance spectroscopy (MRS) in Hippocampus region was carried out in 5 patients of the treatment group. RESULTS: Verbal instant recall scores, symbol digit modalities test (SDMT) scores and mini-mental state examination (MMSE) total scores in the treatment group were improved significantly after treatment as compared with those in the control group (P < 0.05). CONCLUSION: Nimodipine can improve memory ability as well as attention ability of the patients with MCI to a certain extent and make the general cognition function improved.

Aged↗
PubMed2005

[Effect of Ginkgo biloba extract on neuronal apoptosis in rabbit with kaolin-induced syringomyelia].

OBJECTIVE: To evaluate the effect of Ginkgo biloba extract (GBE) on neuronal apoptosis in rabbits with kaolin-induced syringomyelia. METHODS: Twenty-four of 30 Chinese white rabbits were subjected to injection of 25% kaolin mixed with equal volume (0.6 ml) of cerebrospinal fluid drawn from the cisterna magna under ketamine anesthesia. Twelve of these 24 rabbits then received intravenous injection of 5 ml of GBE (5 ml/days for 14 days, GBE treatment group) while the other 12 were treated with the same amount of saline administered in similar manner (saline group). The 6 rabbits without kaolin treatment received a sham operation to serve as the control group. At different time points after the operation, the rabbits were killed and the spinal cord samples examined by immunohistochemistry. RESULTS: Histologically, ischemia and edema in the cervical cord of rabbits in GBE treatment group were less severe than those in saline group. TUNEL-positive and bax-positive neurons were less numerous in GBE treatment group than in saline group, and the former group showed more Bcl-2-positive neurons. The number of apoptotic neurons reached the peak level on day 7 after kaolin injection. CONCLUSION: GBE can ameliorate kaolin-induced hydrocephalus in the upper cervical cord and inhibit kaolin-induced neuron apoptosis.

Animals↗
PubMed2005

[Proteomic comparison between human cerebellums and frontal lobes].

OBJECTIVE: To compare the results of proteomics between the cerebellum and frontal lobe of the aged. METHOD: Proteins were isolated from human cerebellums and frontal lobes and separated by two-dimensional (2D) gel electrophoresis. The proteins were then stained with silver or colloidal coomassie blue to produce a high-resolution map of the proteome. Selected proteins from this map were in-gel digested with trypsin and the resulting tryptic peptides were analyzed by MALDI-TOF mass spectrometry and MALDI TOF/TOF tandem mass spectrometry. The mass spectrometric data were used to identify the proteins through searches of the SWISSPROT protein sequence database. RESULTS: Three up-regulated protein spots in 2D gels of cerebellums were found as compared with those of frontal lobes. These protein spots were identified as antioxidant protein 2, creatine kinase precursor, fructose-bisphosphate aldolase C. Two down-regulated proteins in cerebellums were identified as pyruvate kinase M1 isozyme and glial fibrillary acidic protein. 30 common proteins, the expressions of which were not altered between cerebellums and frontal lobes, were also identified. CONCLUSIONS: These data will be used for future studies of differential protein expression in neurological disorders. Some proteins are useful for discovering the molecular mechanisms of degenerative dementia and brain aging.

Aged↗
PubMed2005

[A preliminary proteomic analysis of tauopathies].

OBJECTIVE: To investigate the molecular mechanisms of tauopathies. Comparative proteomic analysis of brain proteins was employed to study 4 patients with tauopathies as compared with 4 controls. METHODS: The brains of subjects who died without clinical or pathological involvement of nervous system and brains of patients with tauopathies were obtained at autopsy. The brain proteins were run by immobilized pH gradient (IPG) isoelectric focusing electrophoresis as the first dimension, and then run by vertical SDS-PAGE as the second dimension. The maps were visualized by silver staining or colloidal coomassie blue and analyzed with Image Master 2D Elite software. The proteins of interest were in-gel digested and identified using MALDI-TOF mass spectrometry or MALDI-TOF/TOF tandem mass spectrometry. RESULTS: 18 protein spots were differentially expressed as compared with age-matched nondemented control brains which were identified as glyceraldehyde 3-phosphate dehydrogenase, uracil DNA glycosylase, human superoxide dismutase, isocitrate dehydrogenase subunit, synaptotagmin I, thioredoxin peroxidase 1, glial fibrillary acidic protein, p25 alpha, enoyl coenzyme A hydratase short chain 1, pyridoxine-5'-phosphate oxidase, Mn-superoxide dismutase and alpha enolase, antioxidant protein 2, ferritin heavy chain, glutamate dehydrogenase precursor, peptidyl-prolyl cis-trans isomerase A, serum albumin precursor and dihydropyrimidinase-related protein 2. CONCLUSIONS: We got a number of related-proteins of tauopathies. Some proteins are quite useful for discovering the molecular mechanisms of tauopathies and may be helpful for diagnosis and of treatment tauopathies.

Aged↗
PubMed2004

[Glial abnormalities in progressive supranuclear palsy and corticobasal degeneration].

OBJECTIVE: To study pathologic features of glial cells in progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) and to explore their pathologic significance. METHODS: Brain tissues from 2 cases with PSP and 3 cases with CBD, all confirmed by autopsies, were examined by routine neuropathologic methods, Gallyas-Braak staining and tau immunostaining. Brain tissues from 6 Alzheimer's disease cases, 4 cases with Parkinson's disease and 6 elderly with no neurologic abnormality were used as controls. RESULTS: Gallyas-Braak staining demonstrated tuft-shaped astrocytes and coiled-body oligodendroglial cells in the brain tissues of 2 cases with PSP and 3 cases with CBD. The tuft-shaped astrocytes appeared prominently in the frontal and parietal cortex, basal ganglia and grey matter of the brainstem. The coiled-body oligodendroglial cells were distributed widely in the white matter of the frontal and parietal lobes, basal ganglia, brainstem and cerebellum. However, astrocytic plaques, composed of degenerative stubby processes with radiating arrangement, only appeared in the frontal, parietal and cingular cortex, as well as in the striatum of 3 cases with CBD. The astrocytic plaques and tuft-shaped astrocytes coexisted in the same areas, including parietal and cingular cortex and striatum, in CBD. All these glial abnormalities showed tau-positive immunoreaction not found in control cases. CONCLUSIONS: The tuft-shaped astrocytes and coiled-body oligodendroglial cells are common glial morphologic features of both PSP and CBD. Astrocytic plaques are also characteristically seen in CBD.

Aged↗
PubMed2004

[Two-dimensional electrophoregram for proteomic analysis of rat brain with intrahippocampal amyloid beta injection and normal rat brain].

OBJECTIVE: To investigate the molecular mechanisms of Alzheimer's disease by comparing global protein patterns in two-dimensional electrophoregram (2-DE) of the brain of rats with intrahippocampal amyloid beta injection and normal rats. METHODS: From adult SD rats with intrahippocampal injection of amyloid beta, 200 microg brain proteins were extracted with 9 mol/L urea, 4% CHAPS, 1% DTT, 0.5% CA and a cocktail of protease inhibitors. Immobilized pH gradient (IPG) isoelectric focusing electrophoresis of the extracted proteins was performed to obtain the electrophoretogram of the first dimension, with the second dimension obtained by vertical SDS-PAGE. The electrophoretograms were visualized using silver staining and analyzed with ImageMaster 2D-Elite software. RESULTS: On average, 496 and 491 protein spots could be obtained in the electrophoregraphs for rats with amyloid beta and the control rats, respectively, and 30 of these spots exhibited quantitative changes. Another 11 and 6 spots were exclusively shown on the protein maps for amyloid beta-treated rats and control rats, respectively. CONCLUSION: The differentially displayed proteins in the brain identified between the rats with intrahippocampal amyloid beta injection and control rats may provide further insight into the pathogenesis of Alzheimer's disease and useful clues for developing new drugs for its treatment.

Alzheimer Disease↗
PubMed2004

[Morphological and quantatitive capillary changes in aging human brain].

OBJECTIVE: To investigate morphological changes of capillary in aging brain and explore the role of vascular factor in brain aging. METHODS: Twenty-eight brains of individuals (mean age 65 years) who died without clinical or pathological involvement of nervous system and 6 brains of Alzheimer's disease (AD) patients (mean age 83 years) were obtained at autopsy. Sections from frontal lobe, occipital lobe, striatum and hippocampus of normal subjects and sections from hippocampus of AD patients were used for hematoxylin eosin (HE), lox fast blue (LFB), toluidine blue stains and ulex europaeus agglutinin (UEA) immunostaining. After observations of morphological changes of neuron and capillary, computer-aid image analysis was performed to quantify numerical density and area density of neuron and capillary in frontal lobe, occipital lobe, putamen, CA3 sector of normal subjects and CA3 sector of AD patients. Numerical ratio and area ratio of neuron and capillary were then calculated. Correlations between neuron/capillary ratio and age were estimated using Pearson's correlation test. Difference of neuron/capillary ratio in CA3 sectors between AD patients and advanced aged normal subjects (> 75 years) was analyzed with Student's t-test. RESULTS: Several pathological microvascular changes, including increased tortuosity, looping, bundling, stringing, and effacement of endothelia were seen in aged subjects and more prevalent in AD patients. Numerical ratio and area ratio of neuron and capillary of frontal lobe, occipital lobe and putamen significantly increased with age in normal aging subjects. CONCLUSIONS: Morphological changes and relative decrease in number and capacity of capillary in aging brain may reduce cerebral blood flow and metabolism, and consequently result in functional impairment of aging brain. Vascular factors may play an important role in the development of brain aging.

Adult↗
PubMed2004

[Pathologic diagnosis of non-Alzheimer type dementia].

OBJECTIVE: To characterize histopathologic features of non-Alzheimer type dementia. METHODS: Bodian, Gallyas-Braak silver staining, tau and ubiquitin immunohistochemistry were applied in an analysis of 22 cases of autopsy-proven neurodegenerative dementia. Appearance, distribution and immunoreactivity of neuronal and glial inclusions in the brain were observed. The final histological diagnoses were made according to the pathological criteria for several types of common non-Alzheimer type dementia. RESULTS: Among the 22 cases of neurodegenerative dementia, 12 cases were identified as non-Alzheimer type dementia, including Pick's disease (2 cases), progressive supranuclear palsy (3 cases) and corticobasal degeneration (3 cases), dementia with Lewy bodies (1 case), and Parkinson's disease (3 cases). Another 10 cases consisted of pure Alzheimer's disease (AD, 9 cases) and AD combined with argyrophilic grain disease (1 case). Characteristic neuronal and glial inclusions, such as classical and cortical Lewy body, Pick body, Globous NFTs, astrocytic plaque and tufted astrocyte, argyrophilic grain were found in the brains of non-Alzheimer type dementia. Classical and cortical Lewy bodies were not argyrophilic but were immunoreactive to ubiquitin. Pick bodies, Globous NFTs, astrocytic plaques, tufted astrocytes and argyrophilic grains were all argyrophilic. Pick bodies showed tau and ubiquitin immunoreactivity. However, Globous NFTs, astrocytic plaques, tufted astrocytes, and argyrophilic grains were reactive only to tau immunohistochemistry. CONCLUSIONS: Findings of characteristic neuronal and glial inclusions may help to differentiate non-Alzheimer type dementia from AD, and in conjunction with Gallyas-Braak staining and immunohistochemistry for tau and ubiquitin, to further define histopathologic subcategories of non-Alzheimer type dementia.

Aged↗
PubMed2004

[Neuropsychiatric symptoms in dementia and elderly people in the community: results from the Beijing Dementia Cooperative Study].

OBJECTIVE: To determine the prevalence of neuropsychiatric symptoms in dementia and normal elderly people living in the Chinese community of Beijing. METHODS: A cross-sectional study derived from the Beijing Dementia Cooperative Study was carried out a population survey was carried out on a total of 1540 participants aged 65 years and older living in Beijing city and rural areas. All the individuals and 373 demented elderly people completed a series of neuropsychological examination and the Neuropsychiatric Inventory (NPI). RESULTS: Among the dementia participants, 49.33% had exhibited neuropsychiatric symptoms (35.66% rated as clinically significant), in which 80.4% reported 2 or more disturbances, with depression (23.86%), apathy (21.72%) and anxiety (20.38%) being most common. Of the 1540 normal individuals, 18.25% of them exhibited neuropsychiatric symptoms (6.49% rated as clinically significant), in which 53% reported 2 or more disturbances, with sleepless (10%), depression (8.9%) and anxiety (6.97%) being the most common. CONCLUSION: To our knowledge, this was the first multi-center study on neuropsychiatric disturbances in dementia and cognitive normal elderly people. Neuropsychiatric symptoms occurred mainly in persons with dementia and of clinical severity. Though the neuropsychiatric disturbances reported in cognitive normal individuals were lower and less serious compared to dementia, they should not be neglected. These finding suggested that a screening programme focusing on identifying these symptoms should be included in the physician's diagnostic tools for dementia.

Aged↗
PubMed2004

[An interventional study on amnestic mild cognitive impairment with small dose donepezil].

OBJECTIVE: To observe the effect of small dose donepezil (Aricept) on the cognition status and the changes of metabolites in brain tissue in patients with amnestic mild cognitive impairment (aMCI) in order to find out the effective way to prevent and cure dementia. METHODS: 33 patients with aMCI were selected. There were 21 cases in a treatment group taking 2.5 mg of Aricept daily for 3 months and 12 cases in a control group taking basic internal medicines. Before and after taking the medicine, cognition tests such as clinical memory test, basic IQ test, language fluency test and drawing-clock test were carried out. Before and after treatment, magnetic resonance spectroscopy (MRS) in hippocampus region was carried out in 5 patients of the treatment group. RESULTS: Compared with the results before treatment, the memory IQ test, mini-mental state examination (MMSE) total scores as well as delayed memory scores in the treatment group were improved significantly after treatment. The difference was statistically significant. MRS results indicated that after treatment NAA/Cr and Cho/Cr in hippocampus region did not change significantly and MI/Cr was increased. CONCLUSIONS: 2.5 mg/d of Aricept can improve general cognition function in patients with aMCI as shown by memory IQ and delayed memory scores. The results of MRS indicate that no apparent change of NAA/Cr and increase of MI/Cr imply improvement of memory with Aricept through activating astrocytes, stabilizing neurons and regulating the signal transmission among synapses.

Aged↗
PubMed2003

[Prevalence and characteristics of cerebral amyloid angiopathy in the elderly].

OBJECTIVE: To study the prevalence and clinico-neuropathological characteristics of Cerebral amyloid angiopathy (CAA) in Chinese elderly. METHODS: We examined 362 archived brains of aged Chinese from 60 to 95 years of age using an antibody against beta-amyloid peptide and with Gongo red, Bodian and Luxol fast blue stains. RESULTS: CAA appeared in 114 examined brains and the incidence rate in age groups of 60 - 69, 70 - 79, 80 - 89 and beyond 90 years was 22.1%, 26.7%, 46.5% and 66.7% separately; frontal lobe was the most frequently CAA involved part of brain; CAA may also distribute in subcortical white matter and cerebellum dentatus nucleus; close relationships were found between CAA and multiple cerebrovascular lesions, consequent dementia and Alzheimer disease; without other neuropathological changes, CAA alone may result in dementia. CONCLUSIONS: CAA is a common neuropathological finding in brains of Chinese elderly, with an increased prevalence with age. CAA may distribute in subcortical white matter and cerebellum dentatus nucleus, which have been seldom reported before and may contribute to vascular lesions in these areas. CAA may not only participate in the pathogenesis mechanisms of Alzheimer's disease and vascular dementia, but also result in dementia directly through cerebral hypoperfusion and chronic neuronal ischemia.

Age Factors↗
PubMed2003

[An analysis of the causes of dementia in 383 elderly autopsied cases].

OBJECTIVE: To survey the causes of dementia confirmed by autopsy in the elderly and to have a better understanding of various causes of senile dementia. METHODS: A retrospective study on clinical and pathological diagnosis in 383 cases aged 60 and over with autopsy performed was carried out clinical diagnosis of dementia was based on DSM-IVR, NINCDS-ADRDA and NINCDS-AIREN criteria. Gallyas-Braak staining, Tau and Ubiquitin Immunohistochemistry staining were adopted for diagnosing neurodegenerative dementia and distinguishing various degenerative diseases. RESULTS: Among the 383 aged cases with consecutive autopsy, 78 cases were found to have clinical features and brain pathologic change related to dementia. The incidence of dementia in the aged patients with autopsy was 20.4%. Of all the cases, vascular dementia accounted for 38.5% (30 cases), being the most frequently on countered. Next in order were degenerative dementias including Alzheimer's disease (11 cases) and non-Alzheimer's degenerative dementia (9 cases) including dementia with Lewy bodies, corticobasal degeneration, progressive supranuclear palsy, Pick's disease and idiopathic Parkinson'disease. Degenerative dementias accounted for 25.6% (20 cases). Various medical disorders including hepatic encephalopathy, pulmonary encephalopathy, hypoglycemia with cognitive impairment were also relatively common, they accounted for 20.5% (16 cases). The other less common causes included brain tumor, normal pressure hydrocephalus and subdural hematoma, 12 cases accounted 15.4%. The total accordance rate of clinical and pathologic diagnosis of senile dementia was 64.5%, the accordance rates of medical disorders such as hepatic encephalopathy, pulmonary encephalopathy and brain metastatic tumors were all 100%, the accordance rate of vascular dementia and degenerative dementia was 66.7% and 40% respectively. CONCLUSION: Senile dementia is a clinical syndrome caused by multiple factors. Physician should think of various possible causes of dementia, basing on their clinical history and laboratory results. Promoting autopsy and adopting new pathological techniques would increase the diagnostic accuracy of degenerative dementia.

Age Factors↗