About: Nrf2/Wnt resilience orchestrates rejuvenation of glia-neuron dialogue in Parkinson’s disease

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About: Nrf2/Wnt resilience orchestrates rejuvenation of glia-neuron dialogue in Parkinson’s disease Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Nrf2/Wnt resilience orchestrates rejuvenation of glia-neuron dialogue in Parkinson’s disease
Creator	Marchetti, Bianca
Source	Elsevier; PMC
abstract	Oxidative stress and inflammation have long been recognized to contribute to Parkinson’s disease (PD), a common movement disorder characterized by the selective loss of midbrain dopaminergic neurons (mDAn) of the substantia nigra pars compacta (SNpc). The causes and mechanisms still remain elusive, but a complex interplay between several genes and a number of interconnected environmental factors, are chiefly involved in mDAn demise, as they intersect the key cellular functions affected in PD, such as the inflammatory response, mitochondrial, lysosomal, proteosomal and autophagic functions. Nuclear factor erythroid 2 -like 2 (NFE2L2/Nrf2), the master regulator of cellular defense against oxidative stress and inflammation, and Wingless (Wnt)/β-catenin signaling cascade, a vital pathway for mDAn neurogenesis and neuroprotection, emerge as critical intertwinned actors in mDAn physiopathology, as a decline of an Nrf2/Wnt/β-catenin prosurvival axis with age underlying PD mutations and a variety of noxious environmental exposures drive PD neurodegeneration. Unexpectedly, astrocytes, the so-called “star-shaped” cells, harbouring an arsenal of “beneficial” and “harmful” molecules represent the turning point in the physiopathological and therapeutical scenario of PD. Fascinatingly, “astrocyte’s fil rouge” brings back to Nrf2/Wnt resilience, as boosting the Nrf2/Wnt resilience program rejuvenates astrocytes, in turn (i) mitigating nigrostriatal degeneration of aged mice, (ii) reactivating neural stem progenitor cell proliferation and neuron differentiation in the brain and (iii) promoting a beneficial immunomodulation via bidirectional communication with mDAns. Then, through resilience of Nrf2/Wnt/β-catenin anti-ageing, prosurvival and proregenerative molecular programs, it seems possible to boost the inherent endogenous self-repair mechanisms. Here, the cellular and molecular aspects as well as the therapeutical options for rejuvenating glia-neuron dialogue will be discussed together with major glial-derived mechanisms and therapies that will be fundamental to the identification of novel diagnostic tools and treatments for neurodegenerative diseases (NDs), to fight ageing and nigrostriatal DAergic degeneration and promote functional recovery.
has issue date	2020-08-01(xsd:dateTime)
bibo:doi	10.1016/j.redox.2020.101664
has license	no-cc
sha1sum (hex)	07004c9ca25d03182be9339274084e949b10bf7e
schema:url	https://doi.org/10.1016/j.redox.2020.101664
resource representing a document's title	Nrf2/Wnt resilience orchestrates rejuvenation of glia-neuron dialogue in Parkinson’s disease
has PubMed Central identifier	PMC7395594
schema:publication	Redox Biol
resource representing a document's body	covid:07004c9ca25d03182be9339274084e949b10bf7e#body_text
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