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Background: Expression of neuronal thread protein (NTP), which is considered to be related to neuritic sprouting and neuronal death, may be elevated in brain tissue, cerebrospinal fluid, and even urine in patients with Alzheimer's disease (AD).Objective: In this study, we analyzed the correlation between urine AD-associated NTP (AD7c-NTP) level, and amyloid-β (Aβ) deposition, and clinical symptoms in AD and mild cognitive impairment (MCI).Methods: Twenty-two patients with mild to moderate AD and 8 subjects with MCI were recruited. Aβ deposition was measured with [11C]-labeled Pittsburgh compound B (PiB)-positron emission tomography (PET) in all participants. Urine AD7c-NTP levels were measured using enzyme-linked immunosorbent assay. Mini-Mental State Examination (MMSE) and Neuropsychiatric Inventory (NPI) were used to evaluate cognitive function and behavioral psychological symptoms, respectively.Results: Fourteen (63.6%) of AD patients and 2 (25.0%) of MCI subjects were Aβ positive on PiB-PET. There was a significant difference in urine AD7c-NTP level between Aβ positive (2.27±2.22 ng/ml) and negative (0.55±0.60 ng/ml) subjects (p = 0.018). Using 1.46 ng/ml as a cut-off value, 68.8% of Aβ positive subjects showed elevated urine AD7c-NTP level, and 92.9% of Aβ negative subjects showed normal urine AD7c-NTP level. There were no relationships between urine AD7c-NTP level and MMSE and total NPI scores. However, AD7c-NTP level positively correlated with agitation score on NPI.Conclusions: Urine AD7c-NTP had high specificity and moderate sensitivity in predicting Aβ deposition among patients with cognitive impairment. Furthermore, urine AD7c-NTP level strongly correlated with the symptom of agitation. [ABSTRACT FROM AUTHOR]

Background: Cognition and sleep deficits occur in amnestic mild cognitive impairment (aMCI) and vascular cognitive impairment-no dementia (VCIND). However, how memory and sleep deficits differ between aMCI and VCIND remains unclear.Methods: Fifty aMCI and 50 VCIND patients and 38 sex- and age-matched healthy controls (HCs) were administered the Hopkins Verbal Learning Test-Revised (HVLT-R), Trail Making Test-A/B (TMT-A/B), Wisconsin Card Sorting Test (WCST), Paced Auditory Serial Addition Test (PASAT), Symbol Digit Modalities Test (SDMT), Benton Judgment of Line Orientation (JLO) test, Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS), and Insomnia Severity Index (ISI) to quantify cognitive deficits and subjective sleep disturbance.Results: Compared with VCIND patients, aMCI patients had lower HVLT-R scores for total recall (p < 0.001), delayed recall (p < 0.001) and recognition (p = 0.001), and for total-recall (p = 0.002) and delayed-recall (p < 0.001) semantic clustering ratios (SCRs). However, VCIND patients exhibited more obvious executive dysfunction (TMT-A, p < 0.001; TMT-B, p < 0.001; WCST, p < 0.001), lower information processing speed (PASAT, p = 0.003; SDMT, p < 0.001), and more severe sleep disturbance (PSQI, p < 0.001; ESS, p < 0.001; ISI, p < 0.001). Additionally, sleep quality and efficiency were related to total and delayed recall (all r values from -0.31 to -0.60, p < 0.05) in aMCI and VCIND.Conclusions: aMCI and VCIND differ in cognitive function, memory strategy and sleep impairment; these characteristics are helpful to identify and distinguish patients with very early cognitive impairment. Our results also suggest that memory deficits are associated with sleep disturbance in aMCI and VCIND. [ABSTRACT FROM AUTHOR]

Hydroxysafflor yellow A (HSYA) has angiogenesisregulating and neuro-protective effects, but its effects on vascular dementia (VaD) are unknown. In this study, 30 adult Sprague-Dawley rats were randomly allocated to five groups: normal, sham-operation, VaD alone (bilateral carotid artery occlusion), VaD plus saline (control), and VaD plus HSYA. One week after operation, the HSYA group received one daily tail-vein injection of 0.6 mg/100 g HSYA for two weeks. Five weeks after operation, the spatial memory of all five groups was evaluated by the water maze task, and synaptic plasticity in the hippocampus was assessed by the long-term potentiation (LTP) method. Vascular endothelial growth factor (VEGF) and N-methyl-Daspartic acid receptor 1 (NR1) expression in the hippocampus was detected via Western blot. We found that, compared with the group with VaD alone, the group with HSYA had a reduced escape latency in the water maze ( P < 0.05), and the LTP at CA3-CA1 synapses in the hippocampus was enhanced ( P < 0.05). Western blot in the late-phase VaD group showed slight up-regulation of VEGF and downregulation of NR1 in the hippocampus, while HSYA significantly up-regulated both VEGF and NR1. These results suggested that HSYA promotes angiogenesis and increases synaptic plasticity, thus improving spatial learning and memory in the rat model of VaD. [ABSTRACT FROM AUTHOR]