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The future of neuroprotection in stroke

Journal of Neurology Neurosurgery & Psychiatry, 2020
Investigators acknowledge the limitations of rodent or non-human primate stroke models, hundreds of putative neuroprotectants have been evaluated in preclinical models, but not one has entered the clinical realm.
Á. Chamorro   +4 more
semanticscholar   +1 more source

Neuroprotection in Schizophrenia

The Journal of Clinical Psychiatry, 2006
Longitudinal and structural neuroimaging studies show that patients with schizophrenia that converted to psychosis were found to have progressive gray matter loss in the cortex. Gray matter loss was also associated with functional decline. While the underlying mechanisms of gray matter loss remain uncertain, evidence of improved outcomes suggests ...
L Fredrik, Jarskog, Jeffrey A, Lieberman
openaire   +2 more sources

NEUROPROTECTIVE THERAPIES

Medical Clinics of North America, 1999
Though effective symptomatic therapies for Parkinson's disease exist, currently no treatment is proven to slow the progression of the underlying disease. Our growing understanding of the mechanisms of neuronal models, however, offers hope that neuroprotective strategies will soon be a standard part of the treatment of PD.
D K, Simon, D G, Standaert
openaire   +2 more sources

Neurogenic Neuroprotection

Cellular and Molecular Neurobiology, 2003
1. Stimulation of the rostral-ventromedial pole of the cerebellar fastigial nucleus exerts powerful effects on systemic and cerebral circulation. 2. Excitation of fibers passing through the fastigial nucleus evokes sympathoactivation and increases in arterial pressure. 3.
Eugene V, Golanov, Ping, Zhou
openaire   +2 more sources

Incipient neurovulnerability and neuroprotection in early psychosis.

Psychopharmacology bulletin
The objective of this study was to review the implications of altered regulatory mechanisms of progenitor cell generation and death for neurodevelopment and adult brain functioning in early intervention in schizophrenia and related disorders.
G. Berger, S. Wood, P. McGorry
semanticscholar   +1 more source

Perioperative neuroprotection

Best Practice & Research Clinical Anaesthesiology, 2010
The endpoint of all cerebral injuries like stroke, global cerebral ischemia during cardiac arrest, cardiac, vascular, or brain surgery or head trauma is the inadequate supply of the brain with oxygen and glucose, which triggers a characteristic pathophysiologic cascade leading to neuronal death. Many methods and agents have been investigated to produce
Klaus Ulrich, Klein, Kristin, Engelhard
openaire   +2 more sources

Neuroprotective Therapy

Seminars in Neurology, 1998
Neuroprotective therapy for stroke remains unproven despite its ability to substantially reduce injury in animal stroke models. Based on an understanding of the cascade of biochemical events that follow interruption of blood flow to the brain, various neuroprotective drugs have been tested in clinical studies, but none have been shown to improve ...
S L, Hickenbottom, J, Grotta
openaire   +3 more sources

Strategies for Neuroprotection

Journal of Glaucoma, 2001
While glaucoma may be a better candidate for the implementation of neuroprotective strategies than more acute CNS diseases, the failure of clinical neuroprotective trials in stroke should prompt both clinical and basic researchers studying glaucoma to develop better methods to test these agents in animal models, as well as improve methods to quantify ...
openaire   +2 more sources

Neuroprotection by tetracyclines

Trends in Pharmacological Sciences, 2004
The neuroprotective properties of tetracyclines have been clearly established in rodent models of acute and chronic neurodegeneration during the past few years. Recent findings have provided novel insights into the molecular and cellular mechanisms of protection of neurons and oligodendrocytes by tetracyclines.
María, Domercq, Carlos, Matute
openaire   +2 more sources

Neuroprotection in epilepsy

Epilepsia, 2007
Summary Neuroprotection following status epilepticus should encompass not only the prevention of neuronal death, but also preservation of neuronal and network function. This is critical because these aims are not necessarily equivalent; prevention of neuronal loss, for example, does not inevitably prevent epileptogenesis.
Matthew C Walker
exaly   +3 more sources

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