Journal
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
Volume 69, Issue 11, Pages 1331-1338Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/gerona/glu068
Keywords
PACAP; Learning; Memory
Categories
Funding
- Hungarian National Scientific Grant [PD109099]
- Momentum research project [LP2011/007]
- European Social Fund [TAMOP-4.2.4.A/2-11/1-2012-0001, A2-SZGYA-FOK-13-0003]
- National Brain Research Program [KTIA_NAP_13-2-2014-0006]
- Biotechnology and Biological Sciences Research Council [BB/KO18515/1]
- Biotechnology and Biological Sciences Research Council [BB/K018515/1] Funding Source: researchfish
- BBSRC [BB/K018515/1] Funding Source: UKRI
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With the increase of life span, nonpathological age-related memory decline is affecting an increasing number of people. However, there is evidence that age-associated memory impairment only suspends, rather than irreversibly extinguishes, the intrinsic capacity of the aging nervous system for plasticity (1). Here, using a molluscan model system, we show that the age-related decline in memory performance can be reversed by administration of the pituitary adenylate cyclase activating polypeptide (PACAP). Our earlier findings showed that a homolog of the vertebrate PACAP38 and its receptors exist in the pond snail (Lymnaea stagnalis) brain (2), and it is both necessary and instructive for memory formation after reward conditioning in young animals (3). Here we show that exogenous PACAP38 boosts memory formation in aged Lymnaea, where endogenous PACAP38 levels are low in the brain. Treatment with insulin-like growth factor-1, which in vertebrates was shown to transactivate PACAP type I (PAC1) receptors (4) also boosts memory formation in aged pond snails. Due to the evolutionarily conserved nature of these polypeptides and their established role in memory and synaptic plasticity, there is a very high probability that they could also act as memory rejuvenating agents in humans.
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