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Diabetes and Alzheimer’s disease (AD) place a significant burden on health care systems in the world and its aging populations. These diseases have long been regarded as separate entities; however, advanced glycation end products (AGEs) and the receptors for AGEs (RAGE) may be a link between diabetes and AD. In our study, mice injected with AGEs through stereotaxic surgery showed significant AD-like features behavior showed decreased memory; immunofluorescence showed increased phosphorylated tau and APP. These results suggest links between diabetes and AD. Patients with diabetes are at a higher risk of developing AD, and the possible underlying molecular components of this association are now beginning to emerge.Background and purpose The aggregation of vascular risk factors (VRFs) can aggravate cognitive impairment in stroke-free patients. Metabolites in serum and cerebrospinal fluid (CSF) may irreversibly reflect early functional deterioration. This study evaluated small-molecule metabolites (5% and less then 15%), and a high-risk group (10 years stroke risk ≥ 15%) according to the Framingham stroke risk profile (FSRP) score, which was used to quantify VRFs. We assess the cognitive function of the participants. We semiquantitatively quantified the small molecules using liquid chromatography-tandem mass spectrometry (LC-MS/MS). The correlation between the small molecules and cognitive function, along with VRFs, was investigated to identify key small molecules and possible underlying metabolic pathways. Results When the FSRP scores increased, the cognitive performances of the subjects decreased, specifically the performance regarding the tasks of immediate memory, delayed recall, and executive function. Seven metabo biomarkers of vascular cognitive impairment (VCI) at the early stage. Caffeine metabolism and the TCA cycle may play important roles in the pathophysiology of VRF-associated cognitive impairment.Age-associated impairment of spatial learning and memory (AISLM) presents substantial challenges to our health and society. Increasing evidence has indicated that embryonic exposure to inflammation accelerates the AISLM, and this can be attributable, at least partly, to changed synaptic plasticity associated with the activities of various proteins. However, it is still uncertain whether social psychological factors affect this AISLM and/or the expression of synaptic protein-associated genes. Synaptotagmin-1 (Syt1) and activity-regulated cytoskeleton-associated protein (Arc) are two synaptic proteins closely related to cognitive functions. In this study, pregnant CD-1 mice received daily intraperitoneal injections of lipopolysaccharide (LPS) (50 μg/kg) or normal saline at days 15-17 of gestation, and half of the offspring of each group were then subjected to stress for 28 days in adolescence. The Morris water maze (MWM) test was used to separately evaluate spatial learning and memory at 3 and 15 months of age, while western blotting and RNAscope assays were used to measure the protein and mRNA levels of Arc and Syt1 in the hippocampus. The results showed that, at 15 months of age, control mice had worse cognitive ability and higher protein and mRNA levels of Arc and Syt1 than their younger counterparts. Embryonic exposure to inflammation or exposure to stress in adolescence aggravated the AISLM, as well as the age-related increase in Arc and Syt1 expression. Moreover, the hippocampal protein and mRNA levels of Arc and Syt1 were significantly correlated with the performance in the learning and memory periods of the MWM test, especially in the mice that had suffered adverse insults in early life. Our findings indicated that prenatal exposure to inflammation or stress exposure in adolescence exacerbated the AISLM and age-related upregulation of Arc and Syt1 expression, and these effects were linked to cognitive impairments in CD-1 mice exposed to adverse factors in early life.Appropriate medical management can be an alternative in those patients with submacular cysticercosis in whom achieving good visual outcome with vitreoretinal surgery is not possible. We report the case of a 25-year-old female who presented complaining of blurred vision in her left eye associated with photopsias and metamorphopsias of 3 months duration. Initial visual acuity in the right eye was 20/20 and 20/100 in the left eye. Upon indirect ophthalmoscopy in the left eye, a yellow-white, dome-shaped, elevated lesion with foveal involvement was observed. The rest of the ophthalmological examination proved normal. With clinical findings and images, submacular cysticercosis was diagnosed, and vitreoretinal surgery was suggested. Nevertheless, the patient did not accept the treatment; therefore, medical management was initiated. Central nervous system involvement was ruled out, and treatment with praziquantel and systemic prednisolone was initiated. Cysticercosis was resolved with significant improvement of her symptoms and visual acuity.Galactosialidosis is a rare metabolic disorder resulting from mutations in the CTSA gene. Few studies have reported on the ocular findings of galactosialidosis type IIb in detail. We report on a case of galactosialidosis, the diagnosis of which was suggested by bilateral macular cherry-red spots, which is an indication of lysosomal storage disease. In this case, retinal and systemic dysfunctions were mild. Selleck RG2833 Genetic studies revealed an abnormality of relevant protective proteins, and thus a definitive diagnosis was made. The patient was a 35-year-old man who had blurred vision from young age, but he did not seek any therapy due to good visual acuity. He visited a local clinic after the blurred vision in the left eye worsened and was referred to us for bilateral macular cherry-red spots. He had no family history of note. We observed fine grayish-white deposits in the corneal stroma and fine opacity of the lens. Optical coherence tomography showed a hyperreflective region and a thick bilateral retinal ganglion cell layer. Goldmann perimetry showed focal loss of sensitivity. There was almost no functional decline noted on multifocal electroretinography. Lysosomal storage disease was suspected due to corneal clouding and macular cherry-red spots, and so further evaluation was performed. Though neurological abnormality was mild, we made a diagnosis of galactosialidosis because of decreased activity of β-galactosidase and sialidase. Genetic studies revealed an abnormality of relevant protective proteins. Since the onset was later in life and clinical symptoms were mild, we expect that the ophthalmological findings will remain stable. Long-term observation is necessary for this case.