Author
Listed:
- Andre Fischer
(Picower Institute for Learning and Memory, Massachusetts Institute of Technology
Howard Hughes Medical Institute,
Riken-MIT Neuroscience Research Center, Vassar Street, Bldg 46, Cambridge 02139, USA
Present address: European Neuroscience Institute (ENI), Medical School University Goettingen, Max Planck Society, Grisebach Strasse 5, Goettingen 37077, Germany.)
- Farahnaz Sananbenesi
(Picower Institute for Learning and Memory, Massachusetts Institute of Technology
Howard Hughes Medical Institute,
Riken-MIT Neuroscience Research Center, Vassar Street, Bldg 46, Cambridge 02139, USA
Present address: European Neuroscience Institute (ENI), Medical School University Goettingen, Max Planck Society, Grisebach Strasse 5, Goettingen 37077, Germany.)
- Xinyu Wang
(Picower Institute for Learning and Memory, Massachusetts Institute of Technology
Howard Hughes Medical Institute,
Riken-MIT Neuroscience Research Center, Vassar Street, Bldg 46, Cambridge 02139, USA)
- Matthew Dobbin
(Picower Institute for Learning and Memory, Massachusetts Institute of Technology
Howard Hughes Medical Institute,
Riken-MIT Neuroscience Research Center, Vassar Street, Bldg 46, Cambridge 02139, USA)
- Li-Huei Tsai
(Picower Institute for Learning and Memory, Massachusetts Institute of Technology
Howard Hughes Medical Institute,
Riken-MIT Neuroscience Research Center, Vassar Street, Bldg 46, Cambridge 02139, USA)
Abstract
Neurodegenerative diseases of the central nervous system are often associated with impaired learning and memory, eventually leading to dementia. An important aspect in pre-clinical research is the exploration of strategies to re-establish learning ability and access to long-term memories. By using a mouse model that allows temporally and spatially restricted induction of neuronal loss, we show here that environmental enrichment reinstated learning behaviour and re-established access to long-term memories after significant brain atrophy and neuronal loss had already occurred. Environmental enrichment correlated with chromatin modifications (increased histone-tail acetylation). Moreover, increased histone acetylation by inhibitors of histone deacetylases induced sprouting of dendrites, an increased number of synapses, and reinstated learning behaviour and access to long-term memories. These data suggest that inhibition of histone deacetylases might be a suitable therapeutic avenue for neurodegenerative diseases associated with learning and memory impairment, and raises the possibility of recovery of long-term memories in patients with dementia.
Suggested Citation
Andre Fischer & Farahnaz Sananbenesi & Xinyu Wang & Matthew Dobbin & Li-Huei Tsai, 2007.
"Recovery of learning and memory is associated with chromatin remodelling,"
Nature, Nature, vol. 447(7141), pages 178-182, May.
Handle:
RePEc:nat:nature:v:447:y:2007:i:7141:d:10.1038_nature05772
DOI: 10.1038/nature05772
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Cited by:
- Tharick A. Pascoal & Mira Chamoun & Elad Lax & Hsiao-Ying Wey & Monica Shin & Kok Pin Ng & Min Su Kang & Sulantha Mathotaarachchi & Andrea L. Benedet & Joseph Therriault & Firoza Z. Lussier & Frederic, 2022.
"[11C]Martinostat PET analysis reveals reduced HDAC I availability in Alzheimer’s disease,"
Nature Communications, Nature, vol. 13(1), pages 1-11, December.
- Wen-Chung Liu & Chih-Wei Wu & Pi-Lien Hung & Julie Y. H. Chan & You-Lin Tain & Mu-Hui Fu & Lee-Wei Chen & Chih-Kuang Liang & Chun-Ying Hung & Hong-Ren Yu & I-Chun Chen & Kay L.H. Wu, 2020.
"Environmental Stimulation Counteracts the Suppressive Effects of Maternal High-Fructose Diet on Cell Proliferation and Neuronal Differentiation in the Dentate Gyrus of Adult Female Offspring via Histo,"
IJERPH, MDPI, vol. 17(11), pages 1-15, June.
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