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Stress hormones contribute to metabolic and cognitive dysfunction in insulin
Author(s) -
Stranahan Alexis
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.66.2
Subject(s) - long term potentiation , diabetes mellitus , hippocampus , neuroscience , neurogenesis , hippocampal formation , neuroplasticity , hormone , insulin , cognition , synaptic plasticity , psychology , amygdala , chronic stress , neurotrophic factors , cognitive decline , medicine , endocrinology , dementia , receptor , disease
Multiple organ systems are adversely affected by diabetes, including the brain, which undergoes changes that may increase the risk of cognitive decline. In this talk, I will describe the etiology of cognitive deficits associated with insulin resistant diabetes, using data from humans and rodent models. Certain forms of learning depend on changes in the strength of communication between neurons, a phenomenon known as long‐term potentiation. I will present data to show that the induction of long‐term potentiation is impaired in diabetes models. The adult brain continues to generate new neurons throughout life, particularly in the hippocampus, a brain region involved in learning and memory. In diabetes, the rate of adult neurogenesis is reduced, and structural plasticity among the larger cohort of hippocampal neurons is suppressed. The expression of neurotrophic factors that support structural and functional plasticity is also reduced in rodent models of diabetes. Many of these processes can be reversed by attenuating the increased production of stress hormones in diabetes, raising the possibility that minimizing stress could reduce the incidence of cognitive decline among diabetics.