Department of Neurology
MSC10 5620
Health Sciences Center
1 University of New Mexico
Albuquerque, NM 87131-0001

Administrative Office
Phone: (505) 272-3342
Fax: (505) 272-6692

Clinical Neuroscience Centers

Lomas Center
2211 Lomas Blvd. NE
Phone: (505) 272-3160

Ranjana Poddar Laboratory

Ranjana Poddar

Principal Investigator
Ranjana Poddar, PhD
Research Associate Professor, Department of Neurology
CV and profile (VIVO)

The primary focus of the Ranjana Poddar Laboratory is to evaluate the role of hyperhomocysteinemia, a common metabolic disorder, in the progression of age-associated neurological diseases. Recent work in the laboratory provides compelling evidence that predisposition to even mild hyperhomocysteinemic conditions drastically exacerbate the extent of brain damage in rat models of ischemic stroke.

The etiology of ischemic brain injury is primarily attributed to excessive glutamate release, over activation of NR2B subunit containing N-methyl-D-aspartate receptor (NR2B-NMDAR) and increased Ca2+ influx. Our findings now indicate that in contrast to glutamate, homocysteine-induced neuronal cell death involves a novel-signaling pathway that is mediated through NR2A subunit containing NMDAR (NR2A-NMDAR) stimulation, which generally is thought to promote neuronal survival.

The findings also show that while glutamate-NMDAR stimulation leads to a rapid but transient activation of ERK MAPK (extracellular-signal regulated mitogen activated protein kinase) that plays a role in neuronal survival, homocysteine-NMDAR mediated activation of ERK MAPK is sustained, which leads to neuronal cell death. Additionally, homocysteine dependent neuronal injury is found to involve a novel interplay between ERK and stress activated p38 MAPK that is mediated through AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors. These findings demonstrate that homocysteine triggers unique signaling pathways that act in conjunction with ischemia-induced pathways to enhance the pathology of stroke under hyperhomocysteinemic conditions.

The focus of the current NIH funded project is to determine the long-term pathological consequences of ischemic insult under hyperhomocysteinemic conditions and to evaluate the underlying mechanisms involved in hyperhomocysteinemia-induced exacerbation of ischemic brain damage.