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Biomolecules
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The Contribution of Astrocytes to Neuropathology
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The Contribution of Astrocytes to Neuropathology

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: closed (1 December 2023) | Viewed by 29242

Special Issue Editors

Dr. Glória Queiroz

E-Mail Website
Guest Editor
Laboratory of Pharmacology, Department of Drug Sciences, Faculty of Pharmacy, University of Porto, Porto, Portugal
Interests: astrogliosis; microgliosis; purinergic signaling; brain inflammation; glioblastoma
Special Issues, Collections and Topics in MDPI journals
Dr. Clara Quintas

E-Mail Website
Guest Editor
Laboratory of Pharmacology, Department of Drug Sciences, Faculty of Pharmacy, University of Porto, Porto, Portugal
Interests: microglia-astrocyte communication; brain inflammation; astrogliosis; purinergic signalling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the last 50 years, interest in the study of astrocytes grew exponentially and revealed vital physiological functions such as the formation of the blood–brain barrier, control of synaptic transmission, regulation of blood flow, regulation of energy metabolism and many others contributing to the central nervous system (CNS) homeostasis. Therefore, any astroglial dysfunction discloses its role in the origin, modulation, and resolution of different CNS pathologies.

In neurodegenerative diseases, distinct astrocyte phenotypes are associated with specific stages of the disease, with reactive astrocytes having both protective or detrimental functions, whereas dysfunctional astrocytes by losing their homeostatic functions play an important role in neurodegeneration. In some cases, massive astrogliosis associated with activated microglia may be involved in excessive inflammation and contribute to neurotoxic effects in the course of the disease. By controlling neuronal circuits involved in learning, memory and emotion, dysfunctional astrocytes or changes in the number of functional astrocytes may also be involved in the pathophysiology of psychiatric diseases such as depression, anxiety and schizophrenia.

This Special Issue aims to collect high-quality research and review articles that overview the most recent knowledge of astrocytes' biomolecular mechanisms in order to find new strategies of treatment in neuropathology by targeting these glial cells.

Prof. Dr. Glória Queiroz
Dr. Clara Quintas
Guest Editors

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Keywords

  • dysfunctional astrocytes
  • astrogliosis
  • neurodegeneration
  • neuroinflammation
  • CNS diseases

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Published Papers (6 papers)

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Research

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16 pages, 2490 KiB  
Article
AMPKα1 Deficiency in Astrocytes from a Rat Model of ALS Is Associated with an Altered Metabolic Resilience
by Inês Belo do Nascimento, Gamze Ates, Nathalie Desmet, Pauline Beckers, Ann Massie and Emmanuel Hermans
Biomolecules 2023, 13(8), 1183; https://doi.org/10.3390/biom13081183 - 28 Jul 2023
Viewed by 1659
Abstract
Alterations in the activity of the regulator of cell metabolism AMP-activated protein kinase (AMPK) have been reported in motor neurons from patients and animal models of amyotrophic lateral sclerosis (ALS). Considering the key role played by astrocytes in modulating energy metabolism in the [...] Read more.
Alterations in the activity of the regulator of cell metabolism AMP-activated protein kinase (AMPK) have been reported in motor neurons from patients and animal models of amyotrophic lateral sclerosis (ALS). Considering the key role played by astrocytes in modulating energy metabolism in the nervous system and their compromised support towards neurons in ALS, we examined whether a putative alteration in AMPK expression/activity impacted astrocytic functions such as their metabolic plasticity and glutamate handling capacity. We found a reduced expression of AMPK mRNA in primary cultures of astrocytes derived from transgenic rats carrying an ALS-associated mutated superoxide dismutase (hSOD1G93A). The activation of AMPK after glucose deprivation was reduced in hSOD1G93A astrocytes compared to non-transgenic. This was accompanied by a lower increase in ATP levels and increased vulnerability to this insult, although the ATP production rate did not differ between the two cell types. Furthermore, soliciting the activity of glutamate transporters was found to induce similar AMPK activity in these cells. However, manipulation of AMPK activity did not influence glutamate transport. Together, these results suggest that the altered AMPK responsiveness in ALS might be context dependent and may compromise the metabolic adaptation of astrocytes in response to specific cellular stress. Full article
(This article belongs to the Special Issue The Contribution of Astrocytes to Neuropathology)
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14 pages, 1470 KiB  
Article
LRRK2 Kinase Inhibition Attenuates Astrocytic Activation in Response to Amyloid β1-42 Fibrils
by Alice Filippini, Valentina Salvi, Vincenzo Dattilo, Chiara Magri, Stefania Castrezzati, Robert Veerhuis, Daniela Bosisio, Massimo Gennarelli and Isabella Russo
Biomolecules 2023, 13(2), 307; https://doi.org/10.3390/biom13020307 - 6 Feb 2023
Cited by 6 | Viewed by 2501
Abstract
Intracerebral accumulation of amyloid-β in the extracellular plaques of Alzheimer’s disease (AD) brains represents the main cause of reactive astrogliosis and neuroinflammatory response. Of relevance, leucine-rich repeat kinase 2 (LRRK2), a kinase linked to genetic and sporadic Parkinson’s disease (PD), has been identified [...] Read more.
Intracerebral accumulation of amyloid-β in the extracellular plaques of Alzheimer’s disease (AD) brains represents the main cause of reactive astrogliosis and neuroinflammatory response. Of relevance, leucine-rich repeat kinase 2 (LRRK2), a kinase linked to genetic and sporadic Parkinson’s disease (PD), has been identified as a positive mediator of neuroinflammation upon different inflammatory stimuli, however its pathogenicity in AD remains mainly unexplored. In this study, by using pharmacological inhibition of LRRK2 and murine primary astrocytes, we explored whether LRRK2 regulates astrocytic activation in response to amyloid-β1-42 (Aβ1-42). Our results showed that murine primary astrocytes become reactive and recruit serine 935 phosphorylated LRRK2 upon Aβ1-42 fibril exposure. Moreover, we found that pharmacological inhibition of LRRK2, with two different kinase inhibitors, can attenuate Aβ1-42-mediated inflammation and favor the clearance of Aβ1-42 fibrils in astrocytes. Overall, our findings report that LRRK2 kinase activity modulates astrocytic reactivity and functions in the presence of Aβ1-42 deposits and indicate that PD-linked LRRK2 might contribute to AD-related neuroinflammation and pathogenesis. Full article
(This article belongs to the Special Issue The Contribution of Astrocytes to Neuropathology)
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15 pages, 2125 KiB  
Article
The Matricellular Protein Hevin Is Involved in Alcohol Use Disorder
by Amaia Nuñez-delMoral, Paula C. Bianchi, Iria Brocos-Mosquera, Augusto Anesio, Paola Palombo, Rosana Camarini, Fabio C. Cruz, Luis F. Callado, Vincent Vialou and Amaia M. Erdozain
Biomolecules 2023, 13(2), 234; https://doi.org/10.3390/biom13020234 - 25 Jan 2023
Cited by 1 | Viewed by 2723
Abstract
Astrocytic-secreted matricellular proteins have been shown to influence various aspects of synaptic function. More recently, they have been found altered in animal models of psychiatric disorders such as drug addiction. Hevin (also known as Sparc-like 1) is a matricellular protein highly expressed in [...] Read more.
Astrocytic-secreted matricellular proteins have been shown to influence various aspects of synaptic function. More recently, they have been found altered in animal models of psychiatric disorders such as drug addiction. Hevin (also known as Sparc-like 1) is a matricellular protein highly expressed in the adult brain that has been implicated in resilience to stress, suggesting a role in motivated behaviors. To address the possible role of hevin in drug addiction, we quantified its expression in human postmortem brains and in animal models of alcohol abuse. Hevin mRNA and protein expression were analyzed in the postmortem human brain of subjects with an antemortem diagnosis of alcohol use disorder (AUD, n = 25) and controls (n = 25). All the studied brain regions (prefrontal cortex, hippocampus, caudate nucleus and cerebellum) in AUD subjects showed an increase in hevin levels either at mRNA or/and protein levels. To test if this alteration was the result of alcohol exposure or indicative of a susceptibility factor to alcohol consumption, mice were exposed to different regimens of intraperitoneal alcohol administration. Hevin protein expression was increased in the nucleus accumbens after withdrawal followed by a ethanol challenge. The role of hevin in AUD was determined using an RNA interference strategy to downregulate hevin expression in nucleus accumbens astrocytes, which led to increased ethanol consumption. Additionally, ethanol challenge after withdrawal increased hevin levels in blood plasma. Altogether, these results support a novel role for hevin in the neurobiology of AUD. Full article
(This article belongs to the Special Issue The Contribution of Astrocytes to Neuropathology)
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Review

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22 pages, 2181 KiB  
Review
Astrocytes: The Stars in Neurodegeneration?
by Katarina Stoklund Dittlau and Kristine Freude
Biomolecules 2024, 14(3), 289; https://doi.org/10.3390/biom14030289 - 28 Feb 2024
Cited by 12 | Viewed by 4409
Abstract
Today, neurodegenerative disorders like Alzheimer’s disease (AD), Parkinson’s disease (PD), frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) affect millions of people worldwide, and as the average human lifespan increases, similarly grows the number of patients. For many decades, cognitive and motoric decline [...] Read more.
Today, neurodegenerative disorders like Alzheimer’s disease (AD), Parkinson’s disease (PD), frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) affect millions of people worldwide, and as the average human lifespan increases, similarly grows the number of patients. For many decades, cognitive and motoric decline has been explained by the very apparent deterioration of neurons in various regions of the brain and spinal cord. However, more recent studies show that disease progression is greatly influenced by the vast population of glial cells. Astrocytes are traditionally considered star-shaped cells on which neurons rely heavily for their optimal homeostasis and survival. Increasing amounts of evidence depict how astrocytes lose their supportive functions while simultaneously gaining toxic properties during neurodegeneration. Many of these changes are similar across various neurodegenerative diseases, and in this review, we highlight these commonalities. We discuss how astrocyte dysfunction drives neuronal demise across a wide range of neurodegenerative diseases, but rather than categorizing based on disease, we aim to provide an overview based on currently known mechanisms. As such, this review delivers a different perspective on the disease causes of neurodegeneration in the hope to encourage further cross-disease studies into shared disease mechanisms, which might ultimately disclose potentially common therapeutic entry points across a wide panel of neurodegenerative diseases. Full article
(This article belongs to the Special Issue The Contribution of Astrocytes to Neuropathology)
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20 pages, 1533 KiB  
Review
Cellular Pathogenesis of Hepatic Encephalopathy: An Update
by Kaihui Lu
Biomolecules 2023, 13(2), 396; https://doi.org/10.3390/biom13020396 - 19 Feb 2023
Cited by 24 | Viewed by 13382
Abstract
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome derived from metabolic disorders due to various liver failures. Clinically, HE is characterized by hyperammonemia, EEG abnormalities, and different degrees of disturbance in sensory, motor, and cognitive functions. The molecular mechanism of HE has not been [...] Read more.
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome derived from metabolic disorders due to various liver failures. Clinically, HE is characterized by hyperammonemia, EEG abnormalities, and different degrees of disturbance in sensory, motor, and cognitive functions. The molecular mechanism of HE has not been fully elucidated, although it is generally accepted that HE occurs under the influence of miscellaneous factors, especially the synergistic effect of toxin accumulation and severe metabolism disturbance. This review summarizes the recently discovered cellular mechanisms involved in the pathogenesis of HE. Among the existing hypotheses, ammonia poisoning and the subsequent oxidative/nitrosative stress remain the mainstream theories, and reducing blood ammonia is thus the main strategy for the treatment of HE. Other pathological mechanisms mainly include manganese toxicity, autophagy inhibition, mitochondrial damage, inflammation, and senescence, proposing new avenues for future therapeutic interventions. Full article
(This article belongs to the Special Issue The Contribution of Astrocytes to Neuropathology)
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14 pages, 1107 KiB  
Review
A Focus on Astrocyte Contribution to Parkinson’s Disease Etiology
by Giselle Prunell and Silvia Olivera-Bravo
Biomolecules 2022, 12(12), 1745; https://doi.org/10.3390/biom12121745 - 24 Nov 2022
Cited by 11 | Viewed by 3310
Abstract
Parkinson’s disease (PD) is an incurable neurodegenerative disease of high prevalence, characterized by the prominent death of dopaminergic neurons in the substantia nigra pars compacta, which produces dopamine deficiency, leading to classic motor symptoms. Although PD has traditionally been considered as a neuronal [...] Read more.
Parkinson’s disease (PD) is an incurable neurodegenerative disease of high prevalence, characterized by the prominent death of dopaminergic neurons in the substantia nigra pars compacta, which produces dopamine deficiency, leading to classic motor symptoms. Although PD has traditionally been considered as a neuronal cell autonomous pathology, in which the damage of vulnerable neurons is responsible for the disease, growing evidence strongly suggests that astrocytes might have an active role in the neurodegeneration observed. In the present review, we discuss several studies evidencing astrocyte implications in PD, highlighting the consequences of both the loss of normal homeostatic functions and the gain in toxic functions for the wellbeing of dopaminergic neurons. The revised information provides significant evidence that allows astrocytes to be positioned as crucial players in PD etiology, a factor that needs to be taken into account when considering therapeutic targets for the treatment of the disease. Full article
(This article belongs to the Special Issue The Contribution of Astrocytes to Neuropathology)
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