Sirtuins (SIRTs) took their name from Sir2 (silent information regulator 2), NAD+ dependent histone deacetylase which has been shown to slow down replicative aging in yeast. In mammals, there are seven orthologues of yeast Sir2, called SIRT1 - SIRT7, whose presence has been demonstrated in many tissues and organs, including the central nervous system (CNS). Even if not all of them are used to silence transcription, they all have a common molecular mechanism of substrate targeting, through deacetylation, deacylation, or using demyristoylase (SIRT2), ribosyltransferase (SIRT4 and SIRT6), and demanlonylase and desuccinylase (SIRT5), all utilizing NAD+ as a co-substrate. Mammalian SIRTs can have a different subcellular location, chemical structure, or target proteins, yet they are activated mainly by calorie restriction leading to increased concentration of NAD+, i.e., the same way as yeast Sir2.
Calorie restriction has been linked to extension of lifespan and reduction of the risk of neurodegenerative diseases in experimental model systems. Several signaling pathways have been indicated to underlie the beneficial effects of calorie restriction, among which the sirtuin family has been suggested to play a central role. SIRTs regulate brain activity influencing neuroendocrine functions, synaptic plasticity and cognitive processes. There is also connection between the central control of energy homeostasis and reproduction, in which SIRTs participate. Thus, preserved brain homeostasis enables anti-aging effects of SIRTs outside the CNS.
We are seeking manuscripts including but not limited to the mechanisms and/or the implications of SIRTs crosstalk at the level of neurons and neuroglial cells (astrocytes, microglial cells, ependymal cells, and oligodendrocytes) in the context of brain homeostasis. SIRTs and blood brain barrier function studies are also welcome. Both animal and human studies are suitable in this topic, especially dealing with pathophysiology and looking for new treatments. We prefer original research papers but in depth reviews will also be considered.
Examples of in-scope papers include: 1) SIRTs in brain development and senescence; 2) SIRTs and neurodegeneration; 3) SIRTs in modulation of synaptic plasticity; 4) SIRTs and normal cognitive functions of the brain; 5) bioavailability of nutrients and drugs influencing SIRTs activity and the blood brain barrier.
Please note that abstract submission is not mandatory. Interested individuals and research groups are welcome to submit their manuscript to this Research Topic without submitting an abstract beforehand.
Sirtuins (SIRTs) took their name from Sir2 (silent information regulator 2), NAD+ dependent histone deacetylase which has been shown to slow down replicative aging in yeast. In mammals, there are seven orthologues of yeast Sir2, called SIRT1 - SIRT7, whose presence has been demonstrated in many tissues and organs, including the central nervous system (CNS). Even if not all of them are used to silence transcription, they all have a common molecular mechanism of substrate targeting, through deacetylation, deacylation, or using demyristoylase (SIRT2), ribosyltransferase (SIRT4 and SIRT6), and demanlonylase and desuccinylase (SIRT5), all utilizing NAD+ as a co-substrate. Mammalian SIRTs can have a different subcellular location, chemical structure, or target proteins, yet they are activated mainly by calorie restriction leading to increased concentration of NAD+, i.e., the same way as yeast Sir2.
Calorie restriction has been linked to extension of lifespan and reduction of the risk of neurodegenerative diseases in experimental model systems. Several signaling pathways have been indicated to underlie the beneficial effects of calorie restriction, among which the sirtuin family has been suggested to play a central role. SIRTs regulate brain activity influencing neuroendocrine functions, synaptic plasticity and cognitive processes. There is also connection between the central control of energy homeostasis and reproduction, in which SIRTs participate. Thus, preserved brain homeostasis enables anti-aging effects of SIRTs outside the CNS.
We are seeking manuscripts including but not limited to the mechanisms and/or the implications of SIRTs crosstalk at the level of neurons and neuroglial cells (astrocytes, microglial cells, ependymal cells, and oligodendrocytes) in the context of brain homeostasis. SIRTs and blood brain barrier function studies are also welcome. Both animal and human studies are suitable in this topic, especially dealing with pathophysiology and looking for new treatments. We prefer original research papers but in depth reviews will also be considered.
Examples of in-scope papers include: 1) SIRTs in brain development and senescence; 2) SIRTs and neurodegeneration; 3) SIRTs in modulation of synaptic plasticity; 4) SIRTs and normal cognitive functions of the brain; 5) bioavailability of nutrients and drugs influencing SIRTs activity and the blood brain barrier.
Please note that abstract submission is not mandatory. Interested individuals and research groups are welcome to submit their manuscript to this Research Topic without submitting an abstract beforehand.