First, GFAP is a marker for astrocytes and neuronal precursor cells since astrocytes arise from that population as well, and all astrocytes will be positive for GFAP (although basal astrocytes have a lower level). Induction of GFAP, with higher gene expression and protein level is ONE indication of astrocyte reactivity (also known as a pan reactive marker), but does not tell you the function of the cells. Therefore, you could have induction of GFAP but the cells could either be protective or harmful depending on the signaling pathways such as NFkB.

As for the role of GFAP-positive astrocytes in disorders, that question is still mostly unanswered. However, it is known that astrocytes are inherently neuroprotective and during stressful conditions such as Parkinson's or Alzheimer's disease there is an induction of GFAP and what is known as A1 or harmful astrocytes that can secrete a harmful factor that induces neurotoxicity (potentially some inflammatory factor, but hasn't been determined as of yet). This manuscript is a major finding in astrocyte reactivity for neurodegeneration:

Article Neurotoxic reactive astrocytes are induced by activated microglia

But check out the paper that I linked below that shows you can change astrocyte reactivity to either protective or harmful depending on the stimulus given:

http://www.jimmunol.org/content/191/10/5204.long

Hope this helps answer your question to a point.

First, GFAP is a marker for astrocytes and neuronal precursor cells since astrocytes arise from that population as well, and all astrocytes will be positive for GFAP (although basal astrocytes have a lower level). Induction of GFAP, with higher gene expression and protein level is ONE indication of astrocyte reactivity (also known as a pan reactive marker), but does not tell you the function of the cells. Therefore, you could have induction of GFAP but the cells could either be protective or harmful depending on the signaling pathways such as NFkB.

As for the role of GFAP-positive astrocytes in disorders, that question is still mostly unanswered. However, it is known that astrocytes are inherently neuroprotective and during stressful conditions such as Parkinson's or Alzheimer's disease there is an induction of GFAP and what is known as A1 or harmful astrocytes that can secrete a harmful factor that induces neurotoxicity (potentially some inflammatory factor, but hasn't been determined as of yet). This manuscript is a major finding in astrocyte reactivity for neurodegeneration:

Article Neurotoxic reactive astrocytes are induced by activated microglia

But check out the paper that I linked below that shows you can change astrocyte reactivity to either protective or harmful depending on the stimulus given:

http://www.jimmunol.org/content/191/10/5204.long

Hope this helps answer your question to a point.

Thanks you Matthew L Neal for the reply and this reference. I will have a look at it.

Are astrocytes 'Neurotoxic ones' if they scavenge axotomized CNS neurons? ... induced by activated microglia? ... in an "inflammatory" microenvironment?

Sorry for them.

What's the use of an axotomized CNS neuron? What proves it's the astrocyte or some undetermined astrocytic factor that injures axons & oligodendrocytes in a cryptogenic inflammatory environment? - instead of the untraced agent that produced the latter?

Please be so kind as to check the reasons for asking these questions given in the addendum.

Thanks Franz Schelling for the reply and this reference.

Thank you, Adnan Khan - and, please, don't fail to check Frommann's, Charcot's, and Dawson's account on the astrocyte's role in the bilateral cord lesions of spinal MS.

Franz Schelling sure i will check.

The validity of the adult human neurogenesis field should be reconsidered in the context of a recent paper.

Sorrells, S. F., et al. (2018). "Human hippocampal neurogenesis drops sharply in children to undetectable levels in adults." Nature 555(7696): 377-381.

Thanks Alan D Springer for the reference.

Hi, Adnan Khan ,

the Real role of GFAP in neurodegenerative disease is not complete understood. For example, althought there is a general belief that GFAP of glial scar prevent recovery of neuronal elements, a recent paper (doi:10.1038/nature17623) shows that actually this astrocyte scar aids the axonal regeneration. Although we find a GFAP increase in some cases like aging, inflammation and several diseases indicating a "negative" role for this protein, we must keep in mind that only a few astrocytes express GFAP along several classes of astrocytes with many different roles innthe brain, so that we need investigate beyond the correlation between GFAP and events where it is encreased. About the role of GFAP in adult neurogenesis, although is well stablished that progenitors cells expressing GFAP are the principal source of adult neurogenesis in forebrain, hippocampal dentate gyrus and subventricular zone, remains largely unknown the role of GFAP in the recent generated neurons (young neurons) in the adult brain, although there is in general a inverse correlation between amount GFAP and neurogenic rate.

bests,

Marcus

Hi, Marcus A Oliveira,

What or who ever showed that there is an adequate neurogenesis after any kind of neuronal disruption in man?

Can "aging, inflammation and several diseases indicating a "negative" role for this [GFAP]" be considered to be topically relevant without having shown the GFAP production is here not a stereotypal reaction to be provoked by all sorts of traumatising, in particular concussive events, as those seen - in distinctive zonal patterns - in neurovascular conflicts?

Thanks Marcus A Oliveira for your answer and reference. Yes, I agree further investigation is needed to elucidate the exact mechanism.

Thanx Franz Schelling for your valuable contributions.