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Alzheimer Disease: HELP
Articles by Yun-Long Ding
Based on 5 articles published since 2010
(Why 5 articles?)

Between 2010 and 2020, Yun Ding wrote the following 5 articles about Alzheimer Disease.
+ Citations + Abstracts
1 Article The items in the Chinese version of the Montreal cognitive assessment basic discriminate among different severities of Alzheimer's disease. 2019

Zhang, Yan-Rong / Ding, Yun-Long / Chen, Ke-Liang / Liu, Yan / Wei, Can / Zhai, Ting-Ting / Wang, Wen-Juan / Dong, Wan-Li. ·Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou, 215000, Jiangsu, China. · Department of Neurology, Jingjiang People's Hospital, the Seventh Affiliated Hospital of Yangzhou University, Jingjiang, 214500, Jiangsu, China. · Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, 200040, China. · Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou, 215000, Jiangsu, China. dwlsz8@163.com. · Department of Neurology, the First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, Jiangsu, China. dwlsz8@163.com. ·BMC Neurol · Pubmed #31684893.

ABSTRACT: BACKGROUND: To determine whether items of the Chinese version of the Montreal Cognitive Assessment Basic (MoCA-BC) could discriminate among cognitively normal controls (NC), and those with mild cognitive impairment (MCI), mild Alzheimer's disease (AD), and moderate-severe (AD), as well as their sensitivity and specificity. METHODS: MCI (n = 456), mild AD (n = 502) and moderate-severe AD (n = 102) patients were recruited from the memory clinic, Huashan Hospital, Shanghai, China. NC (n = 329) were recruited from health checkup outpatients. Five MoCA-BC item scores were collected in interviews. RESULTS: The MoCA-BC orientation test had high sensitivity and specificity for discrimination among MCI, mild AD and moderate-severe AD. The delayed recall memory test had high sensitivity and specificity for MCI screening. The verbal fluency test was efficient for detecting MCI and differentiating AD severity. CONCLUSIONS: Various items of the MoCA-BC can identify MCI patients early and identify the severity of dementia.

2 Article Inhibition of Phosphodiesterase-4 Reverses Aβ-Induced Memory Impairment by Regulation of HPA Axis Related cAMP Signaling. 2018

Xu, Ying / Zhu, Naping / Xu, Wen / Ye, Han / Liu, Kaiping / Wu, Feiyan / Zhang, Meixi / Ding, Yun / Zhang, Chong / Zhang, Hanting / O'Donnell, James / Pan, Jiangchun. ·Brain Institute, School of Pharmacy, Wenzhou Medical University, Wenzhou, China. · Department of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, University at Buffalo, State University of New York, Buffalo, NY, United States. · Pingyang Hospital of Traditional Chinese Medicine, Pingyang, China. · Hangzhou Geriatric Hospital, Hangzhou, China. · Departments of Behavioral Medicine, Psychiatry and Physiology, and Pharmacology, West Virginia University Health Sciences Center, Morgantown, WV, United States. ·Front Aging Neurosci · Pubmed #30087608.

ABSTRACT: Beta amyloid peptides (Aβ) are found to be associated with dysfunction of hypothalamic-pituitary-adrenal axis (HPA axis) that leads to memory and cognitive deficits in patients with Alzheimer's disease (AD). Phosphodiesterase 4 (PDE4) inhibitors increase the intracellular cAMP activities, which may ameliorate cognitive deficits associated with AD. However, it remains unclear whether PDE4-mediated reversal of cognitive impairment in mouse model of AD is related to HPA axis and downstream cAMP-dependent pathway. The present study investigated the effects of PDE4 inhibitor rolipram on Aβ1-42-induced cognitive dysfunction and its underlying mechanisms. The step-down passive avoidance (PA) and Morris water-maze (MWM) tests were conducted 1 week (1 W), 2 months (2 M), and 6 months (6 M) after intracerebroventricular microjection (i.c.v.) of Aβ1-42. The results suggested that memory impairment emerged as early as 1 W, peaked at 2 M, and lasted until 6 M after injection. Chronic treatment with rolipram (0.1, 0.5, 1.0 mg/kg/d, i.p.) for 2 weeks (i.e., treatment started at 1.5 months after Aβ1-42 microinjection) dose-dependently improved memory performance in both MWM and PA tests. Moreover, rolipram reversed the Aβ-induced increases in serum corticosterone (CORT), corticotropin-releasing factor, and glucocorticoid receptors (CRF-R and GR) levels, whereas it decreases in brain-derived neurotropic factor (BDNF) and the ratio of pCREB to CREB expression. These effects of rolipram were prevented by pre-treatment with PKA inhibitor H89. The findings indicated that the protective effects of rolipram against Aβ1-42-induced memory deficits might involve HPA axis and cAMP-CREB-BDNF signaling.

3 Article Informant questionnaire on cognitive decline in the elderly (IQCODE) for assessing the severity of dementia in patients with Alzheimer's disease. 2018

Ding, Yunlong / Niu, Jiali / Zhang, Yanrong / Liu, Wenpeng / Zhou, Yan / Wei, Can / Liu, Yan. ·Department of Neurology, JingJiang People's Hospital, No. 28, Zhongzhou Road, Jingjiang, CN 214500, Jiangsu, China. · Department of Clinical Pharmacy, JingJiang People's Hospital, No. 28, Zhongzhou Road, Jingjiang, CN 214500, Jiangsu, China. · Department of Neurology, Huashan Hospital at Fudan University, No. 12, Urumqi Road, Shanghai, 200040, CN, China. · Department of Neurology, JingJiang People's Hospital, No. 28, Zhongzhou Road, Jingjiang, CN 214500, Jiangsu, China. liuyan151617@163.com. ·BMC Geriatr · Pubmed #29914396.

ABSTRACT: BACKGROUND: The Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) is widely used as a complementary screening tool for dementia. However, there are few studies concerning the efficacy of the IQCODE for assessing the severity of cognitive impairments in patients with Alzheimer's disease (AD). We aimed to evaluate the efficacy of the IQCODE for assessing the severity of dementia in patients with AD. METHODS: According to the clinical dementia rating (CDR), 394 patients with AD were enrolled and classified into three groups: mild, moderate and severe groups. The IQCODE scores of each group were determined by interviewing the informants with the short version of the 16-item IQCODE. The correlations of the IQCODE score with the Mini-Mental State Examination (MMSE), the Mattis Dementia Rating Scale (DRS) and the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) were analysed. Statistical analyses were conducted to examine the differences in the IQCODE scores among the three groups. RESULTS: The validity coefficients of the IQCODE with the MMSE, DRS and ADAS-Cog were - 0.528, - 0.436, and 0.477, respectively. The sensitivity was 66.1%, and the specificity was 59.8% when using a cut-off score of 65 to discriminate between mild-moderate dementia. When 75 was used as the threshold between moderate-severe dementia, the sensitivity and the specificity were 73.9 and 67.7%, respectively. CONCLUSIONS: The IQCODE is moderately effective for assessing the severity of cognitive impairment in patients with AD.

4 Article Biochemical inhibition of the acetyltransferases ATase1 and ATase2 reduces β-secretase (BACE1) levels and Aβ generation. 2012

Ding, Yun / Ko, Mi Hee / Pehar, Mariana / Kotch, Frank / Peters, Noel R / Luo, Yun / Salamat, Shahriar M / Puglielli, Luigi. ·Department of Medicine, University of Wisconsin-Madison, Madison, Wisconsin 53705, USA. ·J Biol Chem · Pubmed #22267734.

ABSTRACT: The cellular levels of β-site APP cleaving enzyme 1 (BACE1), the rate-limiting enzyme for the generation of the Alzheimer disease (AD) amyloid β-peptide (Aβ), are tightly regulated by two ER-based acetyl-CoA:lysine acetyltransferases, ATase1 and ATase2. Here we report that both acetyltransferases are expressed in neurons and glial cells, and are up-regulated in the brain of AD patients. We also report the identification of first and second generation compounds that inhibit ATase1/ATase2 and down-regulate the expression levels as well as activity of BACE1. The mechanism of action involves competitive and non-competitive inhibition as well as generation of unstable intermediates of the ATases that undergo degradation.

5 Article Indirubin-3'-monoxime rescues spatial memory deficits and attenuates beta-amyloid-associated neuropathology in a mouse model of Alzheimer's disease. 2010

Ding, Yun / Qiao, Aimin / Fan, Guo-Huang. ·Department of Veterans Affairs Medical Center, Richmond, VA 23249, USA. ·Neurobiol Dis · Pubmed #20381617.

ABSTRACT: Indirubin and its derivatives have been shown to possess potent inhibitory effects on cyclin-dependent protein kinase 5 and glycogen synthase kinase 3beta, two protein kinases involved in abnormal hyperphosphorylation of tau and amyloid precursor protein processing/beta-amyloid (Abeta) production. Here, we showed that systemic treatment of APP and presenilin 1 (PS1) transgenic mice, a robust Alzheimer's disease (AD) mouse model, with indirubin-3'-monoxime (IMX; 20mg/kg; 3 times weekly), for as little as 2months, significantly attenuated spatial memory deficits. This was accompanied by a marked decrease in several AD-like phenotypes, including Abeta deposition, tau hyperphosphorylation, accumulation of activated microglia and astrocytes around Abeta plaques, and loss of synaptophysin immunoreactivity. These findings suggest that IMX is a potential therapeutic agent to combat AD.