Plasma fibrinogen is associated with cognitive decline and risk for dementia in patients with mild cognitive impairment

This study was aimed to investigate the relationship between plasma fibrinogen level and risk for cognitive decline and dementia in patients with mild cognitive impairment (MCI). Elderly patients with suspected cognitive impairment were screened and evaluated periodically. One hundred and eighty-five patients who met the criteria for MCI were enrolled. Blood coagulation functions and plasma fibrinogen levels were measured at baseline. Hyperfibrinogenaemia was defined as plasma fibrinogen > or =3.0 g/l. Global cognitive function was assessed serially with Mini-Mental State Examination (MMSE). The enrolled patients were followed for 2 years to observe if dementia was developed. There were 185 patients diagnosed as MCI, of which 17 (9.2%) deceased, 15 (8.1%) lost to follow-up, and 68 (36.8%) developed dementia during follow-up. Mean of MMSE score of the enrolled patients declined significantly during follow-up (22.0 +/- 3.0 vs. 18.1 +/- 5.8, p < 0.001). Patients with hyperfibrinogenaemia at baseline had greater MMSE decrement during follow-up than patients with normal fibrinogen level (-5.4 +/- 5.4 vs. -3.5 +/- 4.5, p < 0.05). Linear regression indicated that plasma fibrinogen level was associated with cognitive decline (R = 0.17, p < 0.05). Patients with hyperfibrinogenaemia had an increased risk for dementia and vascular dementia compared with patients with normal level of plasma fibrinogen (log rank test, p < 0.05). There was a trend that hyperfibrinogenaemia also increased risk for dementia of Alzheimer's type (p = 0.061). It can be concluded that plasma fibrinogen level may be associated with cognitive decline, and hyperfibrinogenaemia may increase risk for dementia in patients with MCI.     

The association of antihypertensive medication use with risk of cognitive decline and dementia: a meta-analysis of longitudinal studies

The association of antihypertensive medication use with cognitive decline (including mild cognitive impairment) or dementia (including Alzheimer's disease (AD), vascular dementia (VD) and any dementia) has still been an area of controversy. This study examined the association of antihypertensive medication use with cognitive decline or dementia using a quantitative meta-analysis of longitudinal studies. EMBASE and MEDLINE were searched for articles published up to Feb 2011. All studies that examined the relationship between antihypertensive medication use and the incidence of dementia or cognitive decline were included. Pooled relative risk (RR) was calculated using fixed and random-effects models. Fourteen studies met our inclusion criteria for this meta-analysis. All subjects were without dementia or cognitive impairment at baseline. There were subjects with (32,658) and without (36,905) antihypertensive medication use. The quantitative meta-analysis showed that there was no significant difference in incidence of AD (RR: 0.90, 95% confidence interval (CI): 0.79-1.03), cognitive decline (RR: 0.97; 95% CI: 0.92-1.03) and cognitive impairment (RR: 0.97; 95% CI: 0.92-1.03). The quantitative meta-analysis showed that the subjects with antihypertensive medication use were lower incidence of VD (RR: 0.67, 95% CI: 0.52-0.87) and any dementia (RR: 0.87; 95% CI: 0.77-0.96) than those without. The quantitative meta-analysis showed that antihypertensive medication use could decrease risk of the development of VD and any dementia, but could not decrease that of AD, cognitive decline and cognitive impairment.     

Circulating serologic and molecular biomarkers in malignant melanoma

The worldwide incidence of malignant melanoma has been increasing during the past decade and is a public health concern because this disease accounts for up to 90% of deaths from cutaneous malignancies. It remains a devastating disease with few therapeutic options once in an advanced stage. Current methods of detection, prognostication, and monitoring of melanoma focus on clinical, morphologic, and histopathologic characteristics of measurable tumor. Although this information provides some insight into disease behavior and outcome, melanoma is still an unpredictable disease. Significant effort has been put into finding an informative serologic biomarker. However, the marker remains elusive, and investigations continue. Using the PubMed database, we reviewed the published literature on serologic melanoma biomarkers and present a synopsis of the extensive investigations that have been performed thus far, provide some insight into why most have failed to become incorporated into routine clinical use, and present an overview of innovative methods currently being explored.     

Searching for biomarkers to diagnose dementia

A decrease in the concentration of amyloid beta-protein-42 and an increase in that of tau or phosphorylated tau in addition to volumetry on MRI and amyloid imaging by PET are available biomarkers. However, we need better biomarkers to detect very early stage of Alzheimer disease to develop disease modifying drugs, which should be used 10 or 15 years prior to emergence of clinical symptoms. In terms of biomarkers for other dementing neurodegenerative diseases, including synucleinopathies such as dementia with Lewy bodies and multiple system atrophy, and tauopathies such as progressive supranuclear palsy, corticobasal degeneration, synuclein, TDP-43, progranulin and tau may be candidate proteins for possible biomarkers for these diseases.     

Alzheimer's dementia. Coping with communication decline

Communication difficulties in patients with Alzheimer's dementia are a major source of caregiver strain because of the psychological and interpersonal burden they present. Nurses are in a critical position for understanding the communication decline and providing education and counseling to decrease this burden. In this article, the communication burden of dementia is examined and practical approaches to facilitating communication are discussed so nurses can increase their role in education and counseling regarding Alzheimer's dementia.     

基于18F-FDG PET及主观认知下降问卷-9诊断主观认知下降

目的 观察基于¹⁸F-FDG PET及主观认知下降问卷-9(SCD-Q9)诊断主观认知下降(SCD)的价值。方法 回顾性分析50例SCD患者(SCD组)及49名健康人(对照组)头颅¹⁸F-FDG PET及主观认知下降问卷-9(SCD-Q9)评估结果;对PET图像行全脑体素定量分析,以脑桥为参考计算标准摄取值比值(SUVR),观察SCD组葡萄糖代谢模式,分析SCD组SUVR减低脑区,评估SUVR减低联合SCD-Q9诊断SCD的价值。结果 相比对照组,SCD组左内侧额上回及右侧额上回SUVR显著减低、左侧距状回SUVR显著升高(GRF校正,体素水平P均＜0.01,团簇水平P均＜0.05)。以左内侧额上回+右侧额上回SUVR联合诊断SCD的敏感度、特异度及曲线下面积(AUC)分别为54.00%、77.60%及0.660,进一步联合SCD-Q9分别为86.00%、75.50%及0.840,其间AUC差异有统计学意义(P＜0.05)。结论 ¹⁸F-FDG PET脑代谢显像可显示SCD脑代谢异常模式;联合SCD-Q9有助于诊断SCD。     

主观认知减退影像学研究进展

阿尔茨海默病（AD）是老年期痴呆的最常见类型。早期诊断AD对于延缓病情进展、改善患者预后十分重要。目前AD研究热点已前移到临床前期,即主观认知减退（SCD）阶段,故采用生物学标记预测SCD是否进展为AD十分必要。本文对SCD的影像学研究进展进行综述。     

主观认知下降的MRI研究进展

主观认知下降(subjective cognitive decline,SCD)是阿尔茨海默病的最早症状,发病率较高.由于缺乏客观量化的诊断金标准,SCD的诊断主要通过临床评估,容易导致误诊和延误治疗.本文就结构磁共振、功能磁共振、弥散张量成像和动脉自旋标记在SCD患者的脑结构和功能方面的应用进展进行综述.目前多模态M...     

Reversible cognitive decline accompanies migraine and cluster headaches

Vascular headaches, including migraine, cluster, and migrainous transformation to chronic daily headaches, are disabling. During and shortly after headache intervals, difficulties are reported in concentration, comprehension, and communication, not accounted for by nausea, photophobia, or sonophobia. These interfere with interpersonal relations and performance at work with economic loss. The hypothesis tested and reported here is that cognitive impairments comprise an important part of vascular headache diatheses. One hundred ninety-six otherwise normative subjects suffering from migraine or cluster, but not tension-type, headaches (136 women, 63 men; mean age, 46 years) participated in an outpatient prospective trial. One hundred thirty-three patients had migraine without aura, 39 migraine with aura, 11 periodic cluster (by IHS criteria), and 13 had migrainous transformation into chronic daily headaches. Neuropsychological testing was compared with and without headaches, by combined Mini-Mental Status Examination (MMSE), Cognitive Capacity Screening Examination (CCSE), and Hamilton Depression Rating Scale (HDRS). During headache intervals, significant decline was measured in both CCSE and MMSE scores (P <. 001) without HDRS change in all types of vascular headache and independent of headache severity, which often improved, or associated physical symptoms. Cognitive decline was promptly relieved by serotonin agonists and sleep. Disorders of cerebral serotoninergic projection systems appear to cause these reversible cognitive impairments.     

Hyperinsulinemia and cognitive decline in a middle-aged cohort

OBJECTIVE: Determining modifiable risks factors for cognitive decline and dementia are a public health priority as we seek to prevent dementia. Type 2 diabetes and related disorders such as hyperinsulinemia increase with aging and are increasing in the U.S. population. Our objective was to determine whether hyperinsulinemia is associated with cognitive decline among middle-aged adults without type 2 diabetes, dementia, or stroke in the Atherosclerosis Risk in Communities (ARIC) cohort. RESEARCH DESIGN AND METHODS: Middle-aged adults (aged 45-64 years at baseline) in the ARIC cohort had fasting insulin and glucose assessed between 1987 and 1989. Subjects with dementia, type 2 diabetes, or stroke at baseline were excluded from analysis. Three tests of cognitive function available at baseline and 6 years later were delayed word recall (DWR), digit symbol subtest (DSS), and first letter word fluency (WF). Cross-sectional comparisons and linear regression models were computed for cognitive tests at baseline and change in cognitive test scores to determine whether cognitive function was associated with two measures of insulin resistance, fasting insulin and homeostasis model assessment (HOMA). Linear regression models controlled for age, sex, race, marital status, education level, smoking status, alcohol use, depression, hypertension, and hyperlipidemia. RESULTS: In unadjusted and adjusted analyses, hyperinsulinemia based on fasting insulin and HOMA at baseline was associated with significantly lower baseline DWR, DSS, and WF scores and a greater decline over 6 years in DWR and WF. CONCLUSIONS: Insulin resistance is a potentially modifiable midlife risk factor for cognitive decline and dementia.     

Perioperative cognitive decline in the aging population

Elderly patients who have an acute illness or who undergo surgery often experience cognitive decline. The pathophysiologic mechanisms that cause neurodegeneration resulting in cognitive decline, including protein deposition and neuroinflammation, also play a role in animal models of surgery-induced cognitive decline. With the aging of the population, surgical candidates of advanced age with underlying neurodegeneration are encountered more often, raising concerns that, in patients with this combination, cognitive function will precipitously decline postoperatively. This special article is based on a symposium that the University of California, San Francisco, convened to explore the contributions of surgery and anesthesia to the development of cognitive decline in the aged patient. A road map to further elucidate the mechanisms, diagnosis, risk factors, mitigation, and treatment of postoperative cognitive decline in the elderly is provided.     

Circulating microRNAs as novel and sensitive biomarkers of acute myocardial Infarction

Coronary artery disease and acute myocardial infarction (AMI) are the leading causes of death for both men and women. Serum cardiac-specific troponin level is now used for the "early" diagnosis of AMI. However, due to the "delayed" release of troponin, an earlier, more sensitive and specific biomarker is urgently demanded to further reduce AMI mortality. Recent studies have found that circulating microRNAs (miRNAs) are closely linked to myocardial injury. Due to the cell-specific physiological functions and the stability of miRNAs in plasma, serum, and urine, they are emerging as sensitive biomarkers of AMI. This review summarizes the latest insights into the identification and potential application of plasma and serum miRNAs as novel biomarkers for diagnosis and prognosis of AMI.     

Biological aging processes underlying cognitive decline and neurodegenerative disease

Alzheimer’s disease and related dementias (ADRD) are among the top contributors to disability and mortality in later life. As with many chronic conditions, aging is the single most influential factor in the development of ADRD. Even among older adults who remain free of dementia throughout their lives, cognitive decline and neurodegenerative changes are appreciable with advancing age, suggesting shared pathophysiological mechanisms. In this Review, we provide an overview of changes in cognition, brain morphology, and neuropathological protein accumulation across the lifespan in humans, with complementary and mechanistic evidence from animal models. Next, we highlight selected aging processes that are differentially regulated in neurodegenerative disease, including aberrant autophagy, mitochondrial dysfunction, cellular senescence, epigenetic changes, cerebrovascular dysfunction, inflammation, and lipid dysregulation. We summarize research across clinical and translational studies to link biological aging processes to underlying ADRD pathogenesis. Targeting fundamental processes underlying biological aging may represent a yet relatively unexplored avenue to attenuate both age-related cognitive decline and ADRD. Collaboration across the fields of geroscience and neuroscience, coupled with the development of new translational animal models that more closely align with human disease processes, is necessary to advance novel therapeutic discovery in this realm.