Treatment strategies of age-related memory dysfunction by modulation of neuronal plasticity.
One of the most remarkable features of the mammalian central nervous system is its ability to store large amounts of information for periods approaching a lifetime. However, during the aging process cognitive domains, such as long-term (declarative) memory and working memory decline in some, but by far not all individuals. It is essential to understand the physiological changes that cause memory decline and also to elucidate why preserved memory abilities vary so greatly across individuals and memory tasks. A generally accepted hypothesis has been that long-lasting activity-dependent changes in the efficacy of synaptic transmission in the mammalian brain are considered to be of fundamental importance for the storage of information. There is now a more detailed understanding of the changes in neuronal plasticity during aging at the molecular and systems levels. This review discusses recent findings on age-related changes in neuronal plasticity, which have opened up novel sites of action for therapeutic intervention.
Blank
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Specialized Neuroscience Research Program II, John A Burns School of Medicine, University of Hawaii, Honolulu, HI 96813, USA. tblank@hawaii.edu
Nijholt
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Spiess
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D000109:Acetylcholine / Q000378:metabolism; D000241:Adenosine / Q000378:metabolism; D000375:Aging / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D020746:Calcium Channels, L-Type / Q000378:metabolism; D006801:Humans; D008569:Memory Disorders / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D009414:Nerve Growth Factors / Q000378:metabolism; D009473:Neuronal Plasticity; D015221:Potassium Channels / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
D020746:Calcium Channels, L-Type; D009414:Nerve Growth Factors; D015221:Potassium Channels; D017382:Reactive Oxygen Species; D000241:Adenosine; D000109:Acetylcholine