Jakob Hakon

ORCID: 0000-0003-1079-0141
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About
Contact & Profiles
Research Areas
  • Neural dynamics and brain function
  • Proteoglycans and glycosaminoglycans research
  • Calpain Protease Function and Regulation
  • Glaucoma and retinal disorders
  • Diabetes Treatment and Management
  • Neonatal Health and Biochemistry
  • Transcranial Magnetic Stimulation Studies
  • Functional Brain Connectivity Studies
  • Vagus Nerve Stimulation Research
  • Acute Ischemic Stroke Management
  • Hyperglycemia and glycemic control in critically ill and hospitalized patients
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neuroscience and Neuropharmacology Research
  • Intracerebral and Subarachnoid Hemorrhage Research
  • Traumatic Brain Injury Research
  • Electrolyte and hormonal disorders
  • EEG and Brain-Computer Interfaces

Lund University
2015-2023

Lund Science (Sweden)
2023

Rigshospitalet
2012-2020

Copenhagen University Hospital
2015-2020

Stroke causes direct structural damage to local brain networks and indirect functional distant regions. Neuroplasticity after stroke involves molecular changes within perilesional tissue that can be influenced by regions functionally connected the site of injury. Spontaneous recovery enhanced rehabilitative strategies, which provides experience-driven cell signaling in enhances plasticity. Functional neuroimaging humans rodents has shown spontaneous sensorimotor function is associated with...

10.1016/j.nicl.2017.11.022 article EN cc-by NeuroImage Clinical 2017-12-02

The inflammatory response plays a pivotal role in propagating injury of intracerebral hemorrhage (ICH). Glucagon-like-peptide-1 (GLP-1) is hormone with antidiabetic effect and may also have antiinflammatory properties. Despite consensus that the glucoregulatory action mediated by GLP-1 receptor (GLP-1R), mechanisms brain remain unclear. We investigated long-acting analog, liraglutide, its truncated metabolite, GLP-1(9–36)a from dipeptidyl peptidase-4 (DPP-4) cleavage ICH-induced injury....

10.1038/jcbfm.2012.133 article EN Journal of Cerebral Blood Flow & Metabolism 2012-09-12

Cerebral edema is a common complication following moderate and severe traumatic brain injury (TBI), significant risk factor for development of neuronal death deterioration neurological outcome. To this date, medical approaches that effectively alleviate cerebral after TBI are not available. Glucagon-like peptide-1 (GLP-1) has anti-inflammatory properties on endothelium exerts neuroprotective effects. Here, we investigated the effects GLP-1 secondary TBI. Male Sprague Dawley rats were...

10.1371/journal.pone.0120074 article EN cc-by PLoS ONE 2015-03-30

Following stroke, complete cellular death in the ischemic brain area may ensue, with remaining areas undergoing tissue remodelling to various degrees. Experience-dependent plasticity exerted through an enriched environment (EE) promotes after central nervous system injury, such as stroke. Post-stroke reorganization is modulated by growth inhibitory molecules differentially expressed within hemisphere, like chondroitin sulfate proteoglycans found perineuronal nets (PNNs). PNNs neocortex...

10.1007/s12035-017-0461-2 article EN cc-by Molecular Neurobiology 2017-03-13

Stroke results in local neural disconnection and brain-wide neuronal network dysfunction leading to neurological deficits. Beyond the hyper-acute phase of ischaemic stroke, there is no clinically-approved pharmacological treatment that alleviates sensorimotor impairments. Functional recovery after stroke involves formation new or alternative circuits including existing connections. The type-5 metabotropic glutamate receptor (mGluR5) has been shown modulate brain plasticity function a...

10.1093/brain/awad293 article EN cc-by Brain 2023-08-31

10.1111/ner.13005 article EN Neuromodulation Technology at the Neural Interface 2020-08-01
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