Biomedical subjects

D R Premkumar

Publications and source records attributed to D R Premkumar.

20 records · Page 2Linked to original sources

PubMed1995

Induction of heme oxygenase-1 mRNA and protein in neocortex and cerebral vessels in Alzheimer's disease.

Previous studies demonstrated the specific association of heme oxygenase (HO)-1 protein to the neurofibrillary pathology of Alzheimer's disease (AD). In this study, we used reverse transcription-polymerase chain reaction methods to show the increased expression of HO-1 but not HO-2 mRNA transcripts in cerebral cortex and cerebral vessels from subjects with AD compared with age-matched non-AD controls. Neither the HO-1 nor the HO-2 mRNA levels was altered in the cerebellum, a brain region usually spared from the pathological alterations of AD. There was no clear evidence that the expression of HO-1 in these tissues was related to postmortem interval, cause of death, or the age of the subjects studied. Using immunoblotting methods, we further showed that HO-1 protein content was increased in neocortical and vascular samples from AD subjects compared with controls. Our findings suggest the specific induction of HO-1 mRNA and protein in the cerebral cortex and cerebral vessels but not HO-2 mRNA or protein in association with the pathological lesions of the disease.

Aged↗

PubMedDate not supplied

Molecular aspects of inflammatory and immune responses in Alzheimer's disease.

Recent advances indicate numerous molecular and cellular elements of the immune system are involved in the pathogenesis of Alzheimer's disease. Amyloid beta protein deposition induces many molecules associated with a predominantly local inflammatory response within the brain parenchyma. These responses also provoke the release of immune system mediators including cytokines, which all seem largely to be produced by reactive cells such as astrocytes and microglia. Classical acute phase proteins of the pentraxin and serine protease inhibitor (serpin) families as well as a host of complement proteins and some coagulation factor seem the most intrinsically involved. These secreted molecules display variable binding with the amyloidotic lesions. Although our understanding of the molecular specificity and significance of the interaction of these proteins within the lesions is not replete, the development of unique inhibitors of the inflammatory reactions could provide therapeutic strategies to impede the pathogenetic process. Currently, this appears a more viable option than to inhibit amyloid beta production or modify amyloid beta precursor protein processing, an approach which seems more complex.

Alzheimer Disease↗