Sammendrag
The honey bee is a key neurobiological model for understanding learning and
memory formation. As a highly social invertebrate, moreover, the bee provides
unique opportunities for cutting-edge research on aging and frailty because it
opens up the interface between the individual and the social environment.
Our group at UMB's Department of Animal and Aquacultural Sciences has over the
last five years contributed to a deeper understanding of the regulation of
honey bee lifespan. We have, e.g., shown that aging in worker bees is not a
clear-cut function of chronological age. This is because aging can be
controlled by social signals through a feedback pathway that involves the
systemic hormone juvenile hormone and the gene vitellogenin. Recently, we
started to investigate whether oxidative brain damage, a hallmark of aging,
can be affected by social signals as well. Our preliminary data, obtained from
immunohistochemical staining of 150 brains from 8200 day-old workers,
suggests that this is indeed the case. The proposal presented here outlines
how we intend to move forward in our work to understand the pathology and
social regulation of honey bee brain aging.
Explicitly, we want to take advantage of the fact that we are at the research
forefront in the field of honey bee longevity regulation; mastering a broad
range of key techniques including brain immunohistochemistry, RNA interference
methodology, immuno- and ligand-blot procedures. From this foundation, we will
first dissect the pathology of bee brain aging in collaboration with Dr. Gimsa
(Sub-goal 1). Next, together with Dr. Scheiner, who is an expert in the use of
the bee as a neurobiological model, we will establish how brain aging affects
the bee's sensory sensitivity and cognitive abilities (Sub-goal 2). Finally,
we will determine the extent of which the pathologies mapped under sub-goals 1
and 2 can be controlled, and possibly reversed, by social signals (Subgoal 3).
NFR 171958 - kontraktspartner overfor NFR: UMB/IHA
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Vitenskapelig sammendrag
The honey bee is a key neurobiological model for understanding learning and
memory formation. As a highly social invertebrate, moreover, the bee provides
unique opportunities for cutting-edge research on aging and frailty because it
opens up the interface between the individual and the social environment.
Our group at UMB's Department of Animal and Aquacultural Sciences has over the
last five years contributed to a deeper understanding of the regulation of
honey bee lifespan. We have, e.g., shown that aging in worker bees is not a
clear-cut function of chronological age. This is because aging can be
controlled by social signals through a feedback pathway that involves the
systemic hormone juvenile hormone and the gene vitellogenin. Recently, we
started to investigate whether oxidative brain damage, a hallmark of aging,
can be affected by social signals as well. Our preliminary data, obtained from
immunohistochemical staining of 150 brains from 8200 day-old workers,
suggests that this is indeed the case. The proposal presented here outlines
how we intend to move forward in our work to understand the pathology and
social regulation of honey bee brain aging.
Explicitly, we want to take advantage of the fact that we are at the research
forefront in the field of honey bee longevity regulation; mastering a broad
range of key techniques including brain immunohistochemistry, RNA interference
methodology, immuno- and ligand-blot procedures. From this foundation, we will
first dissect the pathology of bee brain aging in collaboration with Dr. Gimsa
(Sub-goal 1). Next, together with Dr. Scheiner, who is an expert in the use of
the bee as a neurobiological model, we will establish how brain aging affects
the bee's sensory sensitivity and cognitive abilities (Sub-goal 2). Finally,
we will determine the extent of which the pathologies mapped under sub-goals 1
and 2 can be controlled, and possibly reversed, by social signals (Subgoal 3).
NFR 171958 - kontraktspartner overfor NFR: UMB/IHA
Vis fullstendig beskrivelse