Alzheimer is characterized by the presence of senile plaques and neurofibrillary tangles in cortical regions of the brain. The experimental data is taken from Gene Expression Omnibus. A hierarchical Cluster analysis and TreeView were performed to group genes on the basis of the expression pattern. The dynamic change of expression over time and diverse patterns of expression support the concept of a complex local milieu. TreeView allows the organized data to be visualized. List of 24 genes were obtained which showed high expression levels. Three genes, SORL1, APP, and APOE, are suspected to cause Alzheimer's whereas the other 21 genes are related to other diseases but may also be found to be associated with Alzheimer's, and these are TMEM59, CCT4, IGF2R, SFPQ, PRDX3, RNF14, IDS, SSBP1, SYNE2, TXNL4A, STXBP3, SMARCB1, ULK2, AGTPBP1, FABP7, CALB1, H2AFY, COPA, SAP18, ATIC and SYNCRIP.

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Diabetic cardiomyopathy is a distinct clinical entity that produces asymptomatic heart failure in diabetic patients without evidence of coronary artery disease and hypertension. Abnormalities in diabetic cardiomyopathy include: myocardial hypertrophy, impairment of contractile proteins, accumulation of extracellular matrix proteins, formation of advanced glycation end products, and decreased left ventricular compliance. These abnormalities lead to the most common clinical presentation of diabetic cardiomyopathy in the form of diastolic dysfunction.We evaluated the role of various proteins that are likely to be involved in diabetic cardiomyopathy by employing multiple sequence alignment using ClustalW tool and constructed a Phylogenetic tree using functional protein sequences extracted from NCBI. Phylogenetic tree was constructed using Neighbour—Joining Algorithm in bioinformatics approach. These results suggest a causal relationship between altered calcium homeostasis and diabetic cardiomyopathy that implies that efforts directed to normalize calcium homeostasis could form a novel therapeutic approach.

Diabetes mellitus is a multisystem group of disorders associated with insulin resistance, metabolic stress, endothelial and adipose dysfunction and accelerated atherosclerosis. As the different players leading to atherosclerosis are known, the pathogenesis and eventually targets for treatment can be identified. The purpose of this review is to update the newer aspects of pathogenic factors as well as newer putative biomarkers in atherosclerosis. Hyperglycemia causes beta cell dysfunction, which results in impaired insulin secretion, endoplasmic reticulum stress and overproduction of reactive oxygen species. Lipotoxicity, or the accumulation of increased amounts of lipids in non-adipose tissue is found in the insulin producing pancreatic beta cells impairing their function. Gluco-lipotoxicity leads to the production of inflammatory cytokines, which damage the vasculature. Endothelial dysfunction, which occurs due to all these insults can be studied by biochemical alterations and by non-invasive imaging techniques. In addition, epigenetic changes have been identified in the pathogenesis. More recent biomediators were identified to be involved in the process of atherogenesis including adiponectin, leptin, resistin, adropin, visfatin, hepatokines, bone morphogenetic protein, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), families of micro RNAs, extracellular vesicles (exosomes, ectosomes) and a variety of environmental factors. In view of managing conventional risk factors has not prevented atherosclerotic complications, the better understanding the role of pro-and antiatherogenic factors may allow the development of novel drugs to modify them.