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Over 34 million Americans are living with diabetes. An estimated 6.5 million Americans are living with Alzheimer’s disease (AD) and type 2 diabetes mellites (T2DM). Amyloidosis due to aggregation of amyloid-β is key pathogenic event in AD, whereas aggregation of mature islet amyloid polypeptide (IAPP37) in human islet leads to β-cell dysfunction. A hallmark feature of T2DM is the accumulation of islet amyloid polypeptide fibrils in pancreatic islets. Such accumulations form amyloid plaques and cause apoptosis of -cells of islets. 

There are no effective treatments for Alzheimer’s disease (AD), a progressive brain disease that slowly destroys a person’s memory, cognitive skills and ability to carry out the simplest tasks. AD affects more than 5 million individuals in the United States and ranks as the sixth leading cause of death. The ε4 allele of the apolipoprotein-E (APOE) gene is the strongest genetic risk factor for sporadic or late-onset AD. Heterozygous carriers of the ε4 allele are at three-to-four times greater risk; homozygous carriers are at ten times greater risk.

Traumatic brain injury (TBI) represents a major medical, social and economic concern worldwide due to significant mortality – especially among younger populations – and long-term disabilities. Various pathological brain lesions (e.g., intracerebral bleedings, necrotic-ischemic lesions, tissue avulsion) are produced by impacting mechanical forces. Among these, diffuse axonal injury (DAI) is one of the most significant brain lesions typically associated with trauma. However, DAI is not necessarily linked with TBI exposure. Therefore, the term “traumatic axonal injury (TAI)” is commonly used.

Over 32 million Americans are living with Diabetes and newly diagnosed cases of type 1 and type 2 diabetes is increasing. A defining feature of type 2 diabetes mellitus (T2DM) is the accumulation of islet amyloid polypeptide (IAPP) fibrils in pancreatic islets. Such accumulations form amyloid plaques, referred to as islet amyloidosis. Mounting evidence suggests that islet amyloidosis plays a causative role in the development and progression of ß-cell dysfunction in T2DM.

A significant challenge in developing therapies for the treatment and prevention of cancer has been the discovery, selection, and exploitation of antigens.

The discovery and selection of suitable compounds for the treatment and prevention of autoimmune, inflammatory, and pain disorders is a significant challenge. Researchers at National Institute of Aging (NIA) mitigated this issue. They discovered and synthesized numerous novel fatty acid derivatives (novel small molecules) that may ameliorate these conditions and provide treatment options for these disorders. In a relevant rat model, the fatty acid derivatives developed by NIA demonstrated:

Although multidimensional diffusion/relaxation NMR experiments are widely used in materials sciences and engineering applications, preclinical and clinical MRI applications of these techniques were not feasible. Moreover, higher-field MRI scanners posed another obstacle to translation of this NMR method. Their specific absorption rate (SAR) limits the use of multi-echo or CPMG pulse trains, so that the large amounts of data required by these methods cannot be collected in vivo due to exceedingly long scan times.

Inflammatory processes associated with the over-production of tumor necrosis-alpha (TNF-alpha), a potent activator of the immune system accompany numerous neurodegenerative diseases. TNF-alpha has been validated as a drug target with the development of the inhibitors Enbrel and Remicade (fusion antibodies) as prescription medications. Both, however, are large macromolecules that require direct injection and have limited brain access.

Neurites of the central nervous system can be conceptualized as cylindrical pores with finite lengths and radii. In response to physical trauma, axons may assume a “beaded” morphology which alters their ability to conduct electrical impulses, impairing brain function. These microstructural changes are thought to underlie some of the cognitive defects observed in patients with traumatic brain injury (TBI). Current methods for characterizing traumatic brain injury (TBI) cannot provide microstructural detail on the 3-dimensional shape of axonal segments.