Vidhu Mathur
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View article: Targeting C1q prevents microglia-mediated synaptic removal in neuropathic pain
Targeting C1q prevents microglia-mediated synaptic removal in neuropathic pain Open
Activation of spinal microglia following peripheral nerve injury is a central component of neuropathic pain pathology. While the contributions of microglia-mediated immune and neurotrophic signalling have been well-characterized, the phago…
View article: Novel small molecules therapeutics for FTD/ALS reduce TDP43 related pathology
Novel small molecules therapeutics for FTD/ALS reduce TDP43 related pathology Open
Background TDP43 aggregation and mis‐localization is a hallmark of sporadic Amyotrophic Lateral Sclerosis (ALS) and TDP‐related Frontotemporal dementia (FTD‐TDP). Hyperphosphorylated and ubiquitinated cytosolic TDP43 aggregates have been i…
View article: Safety and Target Engagement of Complement C1q Inhibitor ANX007 in Neurodegenerative Eye Disease
Safety and Target Engagement of Complement C1q Inhibitor ANX007 in Neurodegenerative Eye Disease Open
View article: Pharmacokinetic and Target Engagement Measures of ANX007, an Anti-C1q Antibody Fragment, Following Intravitreal Administration in Nonhuman Primates
Pharmacokinetic and Target Engagement Measures of ANX007, an Anti-C1q Antibody Fragment, Following Intravitreal Administration in Nonhuman Primates Open
Following IVT administration, ANX007 distributes to sites within the retina that are relevant to neurodegenerative ophthalmic disease with clear evidence of C1q target engagement. Based on its mechanism of action inhibiting C1q and its dow…
View article: Complement protein C1q is a therapeutic target for neuropathic pain
Complement protein C1q is a therapeutic target for neuropathic pain Open
Activation of spinal microglia following peripheral nerve injury is a central component of neuropathic pain pathology. While the contributions of microglia-mediated immune and neurotrophic signalling have been well-characterized, the phago…
View article: Complement factor C1q mediates sleep spindle loss and epileptic spikes after mild brain injury
Complement factor C1q mediates sleep spindle loss and epileptic spikes after mild brain injury Open
Neuroinflammation after brain injury Traumatic brain injury affects millions of people every year and is a major cause of disability worldwide. Most of the maladaptive outcomes develop months or years later and are thought to be caused by …
View article: Pharmacokinetics and target engagement of intravitreal administration of ANX007, an anti-C1q antibody fragment, in nonhuman primates
Pharmacokinetics and target engagement of intravitreal administration of ANX007, an anti-C1q antibody fragment, in nonhuman primates Open
View article: Acute and late administration of colony stimulating factor 1 attenuates chronic cognitive impairment following mild traumatic brain injury in mice
Acute and late administration of colony stimulating factor 1 attenuates chronic cognitive impairment following mild traumatic brain injury in mice Open
View article: Author Correction: Lipid-droplet-accumulating microglia represent a dysfunctional and proinflammatory state in the aging brain
Author Correction: Lipid-droplet-accumulating microglia represent a dysfunctional and proinflammatory state in the aging brain Open
View article: Ageing hallmarks exhibit organ-specific temporal signatures
Ageing hallmarks exhibit organ-specific temporal signatures Open
View article: Complement factor C1q mediates chronic neuron loss and inflammation post-brain injury
Complement factor C1q mediates chronic neuron loss and inflammation post-brain injury Open
While traumatic brain injury (TBI) acutely disrupts the cortex, most TBI-related disabilities reflect secondary injuries that accrue over time. The thalamus is a likely site of secondary damage because of its reciprocal connections with th…
View article: Author Correction: Lipid-droplet-accumulating microglia represent a dysfunctional and proinflammatory state in the aging brain
Author Correction: Lipid-droplet-accumulating microglia represent a dysfunctional and proinflammatory state in the aging brain Open
View article: Lipid-droplet-accumulating microglia represent a dysfunctional and proinflammatory state in the aging brain
Lipid-droplet-accumulating microglia represent a dysfunctional and proinflammatory state in the aging brain Open
View article: Lipid droplet accumulating microglia represent a dysfunctional and pro-inflammatory state in the aging brain
Lipid droplet accumulating microglia represent a dysfunctional and pro-inflammatory state in the aging brain Open
Microglia become progressively activated and seemingly dysfunctional with age, and genetic studies have linked these cells to the pathogenesis of a growing number of neurodegenerative diseases. Here we report a striking buildup of lipid dr…
View article: Aged blood inhibits hippocampal neurogenesis and activates microglia through VCAM1 at the blood-brain barrier
Aged blood inhibits hippocampal neurogenesis and activates microglia through VCAM1 at the blood-brain barrier Open
An aged circulatory environment can promote brain dysfunction and we hypothesized that the blood-brain barrier (BBB) mediates at least some of these effects. We observe brain endothelial cells (BECs) in the aged mouse hippocampus express a…
View article: Activation of the STING-Dependent Type I Interferon Response Reduces Microglial Reactivity and Neuroinflammation
Activation of the STING-Dependent Type I Interferon Response Reduces Microglial Reactivity and Neuroinflammation Open
View article: Impact of peripheral myeloid cells on amyloid-β pathology in Alzheimer’s disease–like mice
Impact of peripheral myeloid cells on amyloid-β pathology in Alzheimer’s disease–like mice Open
Although central nervous system–resident microglia are believed to be ineffective at phagocytosing and clearing amyloid-β (Aβ), a major pathological hallmark of Alzheimer’s disease (AD), it has been suggested that peripheral myeloid cells …