Although alpha-synuclein is the main constituent of Lewy bodies, cerebrospinal fluid determination on its own does not seem fundamental for the diagnosis of synucleinopathies. We evaluated whether the combination of classical biomarkers, Aβ(1-42) , total tau, phosphorylated tau, and α-synuclein can improve discrimination of Parkinson's disease, dementia with Lewy bodies, Alzheimer's disease, and frontotemporal dementia. Aβ(1-42) , total tau, phosphorylated tau, and α-synuclein were measured in a series of patients with Parkinson's disease (n = 38), dementia with Lewy bodies (n = 32), Alzheimer's disease (n = 48), frontotemporal dementia (n = 31), and age-matched control patients with other neurological diseases (n = 32). Mean α-synuclein levels in cerebrospinal fluid were significantly lower in the pathological groups than in cognitively healthy subjects. An inverse correlation of α-synuclein with total tau (r = -0.196, P < .01) was observed. In the group of patients with Parkinson's disease, Aβ(1-42) , total tau, and phosphorylated tau values were similar to controls, whereas total tau/α-synuclein and phosphorylated tau/α-synuclein ratios showed the lowest values. Cerebrospinal fluid α-synuclein alone did not provide relevant information for Parkinson's disease diagnosis, showing low specificity (area under the curve, 0.662; sensitivity, 94%; specificity, 25%). Instead, a better performance was obtained with the total tau/α-syn ratio (area under the curve, 0.765; sensitivity, 89%; specificity, 61%). Combined determination of α-synuclein and classical biomarkers in cerebrospinal fluid shows differential patterns in neurodegenerative disorders. In particular, total tau/α-synuclein and phosphorylated tau/α-synuclein ratios can contribute to the discrimination of Parkinson's disease. © 2011 Movement Disorder Society.

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Mild cognitive impairment (MCI) is a common condition in the elderly which may remain stable along time (MCI-MCI) or evolve into Alzheimer's disease (MCI-AD) or other dementias. Cerebrospinal fluid (CSF) classical biomarkers, i.e., amyloid-β 1-42 (Aβ1-42), total tau (t-tau), and phosphorylated tau (p-tau) reflect the neuropathological changes taking place in AD brains, thus disclosing the disease in its prodromal phase. With the aim to evaluate the power of each biomarker and/or their combination in predicting AD progression, we have measured CSF Aβ1-40, Aβ1-42, t-tau, and p-tau in patients with AD, MCI-MCI, MCI-AD, and other neurological diseases without dementia (OND) followed up for four years. Aβ1-42 levels were significantly lower in AD and MCI-AD than in MCI-MCI. T-tau and p-tau levels were significantly increased in AD and MCI-AD versus OND and MCI-MCI. The Aβ1-42/Aβ1-40 ratio showed a significant decrease in AD and MCI-AD as compared to MCI-MCI. Both Aβ1-42/t-tau and Aβ1-42/p-tau ratios showed significantly decreased values in AD and MCI-AD with respect to OND and MCI-MCI. Aβ1-42/p-tau ratio was the best parameter for discriminating MCI-AD from MCI-MCI (sensitivity 81%, specificity 95%), being also correlated with the annual change rate in the Mini Mental State Examination annual change rate score (MMSE-ACR, rS = -0.71, p < 0.0001). Survival analysis showed that 81% of MCI with a low Aβ1-42/p-tau ratio (<1372) progressed to AD. The best model of logistic regression analysis retained Aβ1-42 and p-tau (sensitivity 75%, 95%CI: 70-80%; specificity 96%, 95%CI: 94-98%). We can conclude that Aβ1-42 and p-tau reliably predict conversion to AD in MCI patients.

Abstract-Aim of our study was to ascertain, prospectively, whether serum uric acid is a suitable predictor of preeclampsia and/or the delivery of small-for-gestational-age infants in women with gestational hypertension. We screened 206 primiparas, with a singleton pregnancy, referred for recent onset of hypertension. At presentation, we measured serum uric acid, creatinine, blood glucose, hemoglobin and platelet level, and 24-hour proteinuria, as well as office and 24-hour blood pressures. We followed the women until 1 month after delivery and recorded pregnancy outcome. After logistic regression analysis, uric acid resulted a significant predictor of preeclampsia, with an unadjusted odds ratio of 9.1 (95% CI: 4.8 to 17.4; PϽ0.001); after adjustment for age, gestation week, hemoglobin and platelet levels, serum creatinine, office and 24-hour average systolic and diastolic blood pressures, it was 7.1 (95% CI: 3.2 to 15.7; PϽ0.001). Regarding the association between maternal serum uric acid and the chance of giving birth to a small-for-gestational-age infant, the unadjusted odds ratio was 1.7 (95% CI: 1.4 to 2.2; PϽ0.001), and it was 1.6 (95% CI: 1.1 to 2.4; Pϭ0.02) after adjustment. Receiver operating characteristic analysis showed that serum uric acid, at a 309-mol/L cutoff, predicted the development of preeclampsia (area under the curve: 0.955), with 87.7% sensitivity and 93.3% specificity, and the delivery of small-for-gestational-age infants (area under the curve: 0.784) with 83.7% sensitivity and 71.7% specificity.In conclusion, the results of our study show that serum uric acid is a reliable predictor of preeclampsia in women referred for gestational hypertension. (Hypertension. 2011;58:704-708.)Key Words: uric acid Ⅲ preeclampsia Ⅲ gestational hypertension Ⅲ blood pressure Ⅲ small for gestation age H ypertensive disorders complicate Ϸ2% to 10% of all pregnancies. 1,2 Among these, preeclampsia remains one of the largest single causes of maternal and fetal mortality and morbidity, whereas uncomplicated gestational hypertension carries a far better prognosis. Clinical prediction of preeclampsia may facilitate initiation of timely management to avert mortality and morbidity in the mother and infant. Raised serum uric acid (UA) is one of the characteristic findings in preeclampsia. In clinical practice, serum UA determination is considered to be a part of the workup in women with preeclampsia to monitor disease severity and aid management of these women. The association between raised serum UA and preeclamptic pregnancies was first reported almost a century ago. 3 Reduced UA clearance secondary to reduced glomerular filtration rate, increased reabsorption, and decreased secretion may be at the origin of elevated serum levels in women with preeclampsia. 4,5 Several studies have reported a positive correlation between elevated maternal serum UA and adverse maternal and fetal outcomes. 6 -10 A number of studies 11-15 have evaluated several tests and parameters, including UA, during the first or second trimester of...

Plasma profiles of prolactin, growth hormone, adrenocorticotropic hormone (ACTH) and cortisol were evaluated in a group of untreated patients with idiopathic Parkinson's disease and a group of healthy age-matched controls. Plasma integrated concentrations of all hormones except prolactin were significantly lower in the patients as compared with the controls; however, prolactin nocturnal peak concentration was significantly elevated in the patients; nocturnal growth hormone levels were significantly reduced in the Parkinson group; ACTH and cortisol plasma concentrations were also consistently lower during most of the day in the patients with Parkinson's disease. These data confirm the presence of a hypothalamic disturbance in patients with idiopathic Parkinson's disease, which can affect pituitary function.

A role for uric acid in the pathogenesis and progression of renal disease had been proposed almost a century ago, but, too hastily dismissed in the early eighties. A body of evidence, mostly accumulated during the last decade, has led to a reappraisal of the influence of uric acid on hypertension, cardiovascular, and renal disease. The focus of this review will be solely on the relationship between serum uric acid and renal function and disease. We will review experimental evidence derived from animal and human studies, evidence gathered from a number of epidemiological studies, and from the few (up to now) studies of uric-acid-lowering therapy. Some space will be also devoted to the effects of uric acid in special populations, such as diabetics and recipients of kidney allografts. Finally we will briefly discuss the challenges of a trial of uric-acid-lowering treatment, and the recent suggestions on how to conduct such a trial.

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Maternal diabetes has assumed epidemic relevance in recent years and animal studies have provided some evidence that it may cause abnormalities in renal development and a reduction in nephron endowment in the offspring; however, human data are lacking. The renal cortex contains ∼95% of the glomeruli and its volume could be taken as a surrogate measure of glomerular number; based on this assumption, we measured renal cortex volume and in addition, microalbuminuria in a homogeneous sample of 42 children of diabetic (pregestational, n = 13, and gestational, n = 29) mothers, compared with 21 healthy children born of non-diabetic mothers. The offspring of diabetic mothers showed a significant reduction of renal cortex volume and higher albumin excretion compared with controls, possibly attributable to a reduction in the number of nephrons and the difference was statistically significant (P < 0.001). Although further studies on a larger sample are necessary, our preliminary findings suggest that maternal diabetes may affect renal development with sequelae later in life, requiring closer monitoring and follow-up. Furthermore, the importance of strict maternal diabetes management and control must be emphasized.