Mild cognitive impairment (MCI) of the amnestic type is considered to be a transitionary stage between healthy aging and Alzheimer's disease (AD). Previous studies have demonstrated that intrinsic functional connectivity of the default network (DN) is altered in normal aging and AD and impacts both within- and between-network connectivity. Although changes within the DN have been reported in MCI, it remains uncertain how interactions with other large-scale brain networks are altered in this prodromal stage of AD. We investigated within- and between-network connectivity in healthy older adults (HOAs) and older adults with MCI across 3 canonical brain networks: DN, dorsal attention network, and frontoparietal control network. We also assessed how patterns of functional connectivity among the 3 networks predicted cognitive status and age using multivariate partial least squares. A total of 91 MCI and 71 HOA resting-state scans were analyzed from the Alzheimer's Disease Neuroimaging Initiative. There were 3 key findings. First, a circumscribed pattern of greater between-network and interhemispheric connectivity was associated with higher cognitive status in HOAs. Second, for individuals with MCI, cognitive status was positively associated with a more distributed, less-differentiated pattern of intrinsic functional connectivity across the 3 networks. Finally, greater within-network functional connectivity was positively associated with cognitive status for HOAs irrespective of age; however, this compensation-like effect diminished with increasing age for participants with MCI. Although reliable differences between healthy aging and MCI in the intrinsic network architecture of the brain are apparent, these differences emerge as shifting associations between network interactivity, cognitive functioning, and age.

Opsoclonus-myoclonus syndrome (OMS) is a very rare condition with different autoimmune, infectious and paraneoplastic aetiologies or in most cases idiopathic. We report the case of a 75-year-old woman who was admitted in our department in early fall for altered mental status, opsoclonus, multifocal myoclonus, truncal titubation and generalized tremor, preceded by a 5 day prodrome consisting of malaise, nausea, fever and vomiting. Brain computed tomography and MRI scans showed no significant abnormalities and cerebrospinal fluid changes consisted of mildly increased protein content and number of white cells. Work-up for paraneoplastic and autoimmune causes of OMS was negative but serologic tests identified positive IgM and IgG antibodies against West Nile virus (WNV). The patient was treated with Dexamethasone and Clonazepam with progressive improvement of mental status, myoclonus, opsoclonus and associated neurologic signs. Six months after the acute illness she had complete recovery. To our knowledge this is the 14th case of WNV associated OMS reported in the literature so far. We briefly describe the clinical course of the other reported cases together with the different treatment strategies that have been employed.

Hemolytic uremic syndrome is commonly caused by Shiga toxin-producing Escherichia coli (STEC). Up to 15% of individuals with STEC-associated hemorrhagic diarrhea develop hemolytic uremic syndrome (STEC HUS). Hemolytic uremic syndrome (HUS) is a disorder comprising of thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury. The kidney is the most commonly affected organ and approximately half of the affected patients require dialysis. Other organ systems can also be affected including the central nervous system and the gastrointestinal, cardiac, and musculoskeletal systems. Neurological complications include altered mental status, seizures, stroke, and coma. Gastrointestinal manifestations may present as hemorrhagic colitis, bowel ischemia/necrosis, and perforation. Pancreatitis and pancreatic beta cell dysfunction resulting in both acute and chronic insulin dependant diabetes mellitus can occur. Thrombotic microangiopathy (TMA) in cardiac microvasculature and troponin elevation has been reported, and musculoskeletal involvement manifesting as rhabdomyolysis has also been described. Extrarenal complications occur not only in the acute setting but may also be seen well after recovery from the acute phase of HUS. This review will focus on the extrarenal complications of STEC HUS. To date, management remains mainly supportive, and while there is no specific therapy for STEC HUS, supportive therapy has significantly reduced the mortality rate.

Modern sedentary lifestyle with altered dietary habits imposes the risk of human health towards several metabolic disorders such as obesity. The metabolic insults negatively affect the mental health status and quality life of affected individuals. Melatonin is a potent antioxidant with anti-inflammatory and neuroprotective properties. The aim of the present study was to investigate the protective effect of melatonin on the cognitive and neurochemical deficits induced by the high-fat diet (HFD) and alcohol (ALC) alone or in combination (HFD + ALC) in rats. Male Wistar rats were given ALC (3-15% i.e. increased gradually) and HFD for 12 weeks in different experimental groups. After 12 weeks, we found that simultaneous consumption of HFD and ALC exacerbates cognitive dysfunction and neurochemical anomalies. However, melatonin (10 mg/kg/day, i.p.) treatment for four weeks significantly prevented memory deficits, oxidative stress and neuroinflammation in HFD, ALC and HFD + ALC groups. RT-PCR analysis showed down-regulation of nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase-1 (HO-1) in ALC and HFD + ALC groups. Moreover, caspase-3 and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) mRNA expression level were found up-regulated in hippocampus of HFD, ALC and HFD + ALC groups. However, calpain expression was found up-regulated only in the hippocampus of HFD + ALC group. Chronic treatment with melatonin significantly restored the aberrant gene expression level in HFD, ALC and HFD + ALC group. In conclusion, our findings indicated that melatonin can mitigate the HFD and ALC-induced cognitive deficits via attenuation of oxidative stress and calpain-1 dependent as well as independent caspase-3 mediated neuronal cell death.

Altered cholinergic neural transmission is hypothesized to increase susceptibility to cognitive deficits in psychotic disorders such as schizophrenia (SCZ). The nicotinic acetylcholine receptor α5 subunit gene (CHRNA5) is reported to be associated with cognitive function in nicotine-dependent populations and SCZ in non-smoking SCZ patients. Nevertheless, it is still not clear whether the CHRNA5 gene contributes to susceptibility to the cognitive deficits of SCZ without smoking. To further clarify the role of CHRNA5, we designed a two-stage, case-control study to examine the association between CHRNA5 and SCZ and its clinical features adjusted for smoking status in early-onset SCZ patients. A total of 15 tag single nucleotide polymorphisms (SNPs) on CHRNA5 were genotyped in the discovery stage, which included 485 early-onset SCZ patients and 1018 controls, and then, we replicated this association in a confirmatory population of 674 patients and 1886 controls. The rs16969968 SNP was identified as significantly associated with SCZ in both datasets. In addition, the severity of psychotic symptoms and cognitive deficits was assessed using the Positive and Negative Syndrome Scale (PANSS) and the Wisconsin Card Sorting Test (WCST). The rs16969968 SNP was associated with psychotic symptoms in patients and with cognitive function in patients and controls. Our results show that rs16969968 on CHRNA5 is tightly linked to genetic susceptibility, psychotic symptoms and cognitive deficits in SCZ in an early-onset Chinese population, suggesting that CHRNA5 may play an important role in the etiology of SCZ.