Issues of critical importance
Abnormal lipids and cognitive impairment: Several lines of evidence suggest that cholesterol metabolism plays an important role in pathophysiology of demetia, suhc as AD. However, so far the association between L5 and pathogenesis of AD remains unknown. Our hypothesis is that L5 may cause injury or dysfunction of the BBB to enhance the possibilty of neurotoxicity by L5 itself or other toxins. A key point in our research is to determien the role of L5 in AD pthogeneiss, including converion of MCI to AD or severe dementia. Another approach is to examine the synergistic effects of L5 and Ab on Ab-mediated cerebral angiopathy, a pattern of vascular dementia secondary to lucunar strokes. A target of interest is platelets. By activating the NF-kB, the L5-Ab duo can induce platelet aggregation precipitating to ischemic strokes. A novel therapeutic method invloing interfering miR-regulated sugnaling is also being developed.
Molecular mechanisms of high glucose and L5 cause cognitive decline and neuropathy:We aim to investigate the role of inflammatory mediators and macrophage polarization in cognitive decline among diabetic patients and its pathogenesis, investigate the role of electronegative low-density lipoprotein in cognitive decline and its pathogenesis in neurodegenerative diseases including Alzheimer’s disease and persistent hyperglycemia dys-regulates sodium channels expression in sensory and sympathetic ganglion neurons.