Abstract
Ageing is characterized by alterations in brain anatomy and physiology, finally contributing to an impairment in cognitive functions, such as memory. The most relevant observations indicate that senescent-related cognitive decline is not only due to neuronal loss, instead, functional changes occurring over time play a key role. Overall, these modifications are indeed responsible for an altered interneuronal communication that can represent, rather than morphological modifications, the primum movens leading to cognitive decline. Among the age-induced changes underlying alterations in neuronal communication and synaptic plasticity, those related to neurotransmitter/neurotrophin systems and downstream signalling pathways are of great relevance. In particular, considering that protein kinases play a strategic role aimed to convert the extracellular signals into biological responses, functional alterations on kinases may directly contribute to age-dependent neuronal dysfunctions. Within this context, numerous studies point out on several kinases as positive regulators for memory function and suggest that various memory disturbances are the result of a deficit in kinase signalling pathways. Many kinases associated with synaptic function are indeed age-sensitive; in fact, various studies in senescent animals indicate that a reduction in kinases expression/function in some brain areas correlates with ageing and memory decline. In line with these concepts, pharmacological modulation of kinases may lead to neuroprotective effects that can prevent or counteract age-related memory impairment. This review will mainly focus on the age-induced changes on Protein Kinase C (PKC), Protein Kinase A (PKA), Calcium/calmodulin-dependent Protein Kinase (CaMK), Tyrosine Kinase, widely accepted as key actors in signalling pathways associated with memory.
Keywords: Aging, Protein Kinase C, Protein Kinase A, CaM Kinase, Tyrosine Kinase, ELAV, Memory
Current Pharmaceutical Design
Title: Senescence of the Brain: Focus on Cognitive Kinases
Volume: 16 Issue: 6
Author(s): S. Govoni, M. Amadio, F. Battaini and A. Pascale
Affiliation:
Keywords: Aging, Protein Kinase C, Protein Kinase A, CaM Kinase, Tyrosine Kinase, ELAV, Memory
Abstract: Ageing is characterized by alterations in brain anatomy and physiology, finally contributing to an impairment in cognitive functions, such as memory. The most relevant observations indicate that senescent-related cognitive decline is not only due to neuronal loss, instead, functional changes occurring over time play a key role. Overall, these modifications are indeed responsible for an altered interneuronal communication that can represent, rather than morphological modifications, the primum movens leading to cognitive decline. Among the age-induced changes underlying alterations in neuronal communication and synaptic plasticity, those related to neurotransmitter/neurotrophin systems and downstream signalling pathways are of great relevance. In particular, considering that protein kinases play a strategic role aimed to convert the extracellular signals into biological responses, functional alterations on kinases may directly contribute to age-dependent neuronal dysfunctions. Within this context, numerous studies point out on several kinases as positive regulators for memory function and suggest that various memory disturbances are the result of a deficit in kinase signalling pathways. Many kinases associated with synaptic function are indeed age-sensitive; in fact, various studies in senescent animals indicate that a reduction in kinases expression/function in some brain areas correlates with ageing and memory decline. In line with these concepts, pharmacological modulation of kinases may lead to neuroprotective effects that can prevent or counteract age-related memory impairment. This review will mainly focus on the age-induced changes on Protein Kinase C (PKC), Protein Kinase A (PKA), Calcium/calmodulin-dependent Protein Kinase (CaMK), Tyrosine Kinase, widely accepted as key actors in signalling pathways associated with memory.
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Cite this article as:
Govoni S., Amadio M., Battaini F. and Pascale A., Senescence of the Brain: Focus on Cognitive Kinases, Current Pharmaceutical Design 2010; 16 (6) . https://dx.doi.org/10.2174/138161210790883732
DOI https://dx.doi.org/10.2174/138161210790883732 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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