Results 41 to 50 of about 90,697 (359)
Stroke is a major cause of death and adult disability. However, therapeutic options remain limited. Numerous pathways underlie acute responses of brain tissue to stroke.
Qianwen Yang+3 more
semanticscholar +1 more source
Tau exacerbates excitotoxic brain damage in an animal model of stroke
Excitotoxicity contributes to neuronal injury following stroke. Here the authors show that tau promotes excitotoxicity by a post-synaptic mechanism, involving site-specific control of ERK activation, in a mouse model of stroke.
Mian Bi+18 more
doaj +1 more source
A serendipitous pharmacogenetic finding links the vulnerability to developing levodopa-induced dyskinesia to the age of onset of Huntington’s disease. Huntington’s disease is caused by a polyglutamate expansion of the protein huntingtin.
Svetlana A. Ivanova, Anton J. M. Loonen
doaj +1 more source
Delayed treatment with nimesulide reduces measures of oxidative stress following global ischemic brain injury in gerbils [PDF]
Metabolism of arachidonic acid by cyclooxygenase is one of the primary sources of reactive oxygen species in the ischemic brain. Neuronal overexpression of cyclooxygenase-2 has recently been shown to contribute to neurodegeneration following ischemic ...
Alvarez, Dalia+3 more
core +1 more source
Neurodegeneration in multiple sclerosis
Chronic demyelination results in impaired axon metabolism and function, ultimately leading to progressive neurological decline. Neuroprotective strategies aim to protect axons from inflammatory‐mediated destruction, thereby improving axonal integrity and clinical disability (Image created in BioRender.com).
Gabrielle M. Mey+2 more
wiley +1 more source
Ambient but not local lactate underlies neuronal tolerance to prolonged glucose deprivation [PDF]
Neurons require a nearly constant supply of ATP. Glucose is the predominant source of brain ATP, but the direct effects of prolonged glucose deprivation on neuronal viability and function remain unclear.
Mennerick, Steven+3 more
core +2 more sources
There is no pharmacological treatment available to limit progressing neuronal death after cerebral ischemia. Here we show that targeting the interaction of GABAB receptors with CaMKII using a synthetic interfering peptide after an excitotoxic insult in cultured neurons or in brain slices from MCAO‐treated mice restored downregulated GABAB receptor ...
Karthik Balakrishnan+7 more
wiley +1 more source
Bioenergetics and glutamate excitotoxicity
Bioenergetic defects and abnormalities in glutamate neurotransmission have both been proposed to play important roles in neurological diseases of varying chronology, etiology and pathology. Recent experimental evidence suggests an intimate relationship between these two systems.
Greenamyre Jt, Greene Jg
openaire +3 more sources
Imbalance of p75(NTR)/TrkB protein expression in Huntington's disease: Implication for neuroprotective therapies [PDF]
Neuroprotective therapies based on brain-derived neurotrophic factor (BDNF) administration have been proposed for Huntington's disease (HD) treatment. However, our group has recently reported reduced levels of TrkB in HD mouse models and HD human brain ...
Alberch, J.+5 more
core +1 more source
Differential alteration of synaptic versus extrasynaptic NMDARs in P301S mice. Reduced density of synaptic NMDARs in excitatory synapses in the hippocampus of P301S mice at 10 months. NMDARs at excitatory synapses established on pyramidal cell spines and interneurons are significantly reduced in the CA1 region of the hippocampus compared to age‐matched
Rocío Alfaro‐Ruiz+8 more
wiley +1 more source