Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination
Background The dietary consumption of cuprizone–a copper chelator–has long been known
to induce demyelination of specific brain structures and is widely used as model of multiple …
to induce demyelination of specific brain structures and is widely used as model of multiple …
The blood-brain barrier in health and chronic neurodegenerative disorders
BV Zlokovic - Neuron, 2008 - cell.com
The blood-brain barrier (BBB) is a highly specialized brain endothelial structure of the fully
differentiated neurovascular system. In concert with pericytes, astrocytes, and microglia, the …
differentiated neurovascular system. In concert with pericytes, astrocytes, and microglia, the …
Oxidative stress and neurotoxicity
LM Sayre, G Perry, MA Smith - Chemical research in toxicology, 2008 - ACS Publications
There is increasing awareness of the ubiquitous role of oxidative stress in
neurodegenerative disease states. A continuing challenge is to be able to distinguish …
neurodegenerative disease states. A continuing challenge is to be able to distinguish …
Synaptopathy connects inflammation and neurodegeneration in multiple sclerosis
G Mandolesi, A Gentile, A Musella… - Nature Reviews …, 2015 - nature.com
Multiple sclerosis (MS) has long been regarded as a chronic inflammatory disease of the
white matter that leads to demyelination and eventually to neurodegeneration. In the past …
white matter that leads to demyelination and eventually to neurodegeneration. In the past …
The regulation of astrocytic glutamate transporters in health and neurodegenerative diseases
AC Todd, GE Hardingham - International journal of molecular sciences, 2020 - mdpi.com
The astrocytic glutamate transporters excitatory amino acid transporters 1 and 2 (EAAT1 and
EAAT2) play a key role in nervous system function to maintain extracellular glutamate levels …
EAAT2) play a key role in nervous system function to maintain extracellular glutamate levels …
Excitatory amino acid transporters in physiology and disorders of the central nervous system
AR Malik, TE Willnow - International journal of molecular sciences, 2019 - mdpi.com
Excitatory amino acid transporters (EAATs) encompass a class of five transporters with
distinct expression in neurons and glia of the central nervous system (CNS). EAATs are …
distinct expression in neurons and glia of the central nervous system (CNS). EAATs are …
Linking oligodendrocyte and myelin dysfunction to neurocircuitry abnormalities in schizophrenia
Multiple lines of evidence in schizophrenia, from brain imaging, studies in postmortem
brains, and genetic association studies, have implicated oligodendrocyte and myelin …
brains, and genetic association studies, have implicated oligodendrocyte and myelin …
P2X7 receptor blockade prevents ATP excitotoxicity in oligodendrocytes and ameliorates experimental autoimmune encephalomyelitis
Oligodendrocyte death and demyelination are hallmarks of multiple sclerosis (MS). Here we
show that ATP signaling can trigger oligodendrocyte excitotoxicity via activation of calcium …
show that ATP signaling can trigger oligodendrocyte excitotoxicity via activation of calcium …
Neuroinflammation and regulation of glial glutamate uptake in neurological disorders
S Tilleux, E Hermans - Journal of neuroscience research, 2007 - Wiley Online Library
Oxidative stress, neuroinflammation, and excitotoxicity are frequently considered distinct but
common hallmarks of several neurological disorders, including Parkinson's disease …
common hallmarks of several neurological disorders, including Parkinson's disease …
Inflammation triggers synaptic alteration and degeneration in experimental autoimmune encephalomyelitis
D Centonze, L Muzio, S Rossi, F Cavasinni… - Journal of …, 2009 - Soc Neuroscience
Neurodegeneration is the irremediable pathological event occurring during chronic
inflammatory diseases of the CNS. Here we show that, in experimental autoimmune …
inflammatory diseases of the CNS. Here we show that, in experimental autoimmune …