Monday, June 17, 2024

Elucidating the pivotal molecular mechanisms, therapeutic and neuroprotective effects of lithium in traumatic brain injury

You can ask your competent? doctor what has been done with all this earlier research. No knowledge you need to fire your doctor.

I've got 14 posts on lithium back to 2011 and I bet your stroke medical 'professionals' have not done one damn thing. WHOM will create protocols for lithium?

 Elucidating the pivotal molecular mechanisms, therapeutic and neuroprotective effects of lithium in traumatic brain injury

Received: 9 January 2024 Revised: 17 May 2024 Accepted: 26 May 2024
DOI: 10.1002/brb3.3595

Seidu A. Richard1,2
1 Department of Medicine, Princefield
University, Ho, Ghana
2 Institute of Neuroscience, Third Affiliated
Hospital, Zhengzhou University, Zhengzhou,
China
Correspondence
Seidu A. Richard, Department of Medicine,
Princefield University, P. O. Box MA 128,
Ho-Volta Region, Ghana.
Email: gbepoo@gmail.com


Abstract

Introduction: 
 
Traumatic brain injury (TBI) refers to damage to brain tissue by mechan-
ical or blunt force via trauma. TBI is often associated with impaired cognitive abilities,
like difficulties in memory, learning, attention, and other higher brain functions, that
typically remain for years after the injury. Lithium is an elementary light metal that
is only utilized in salt form due to its high intrinsic reactivity. This current review
discusses the molecular mechanisms and therapeutic and neuroprotective effects of
lithium in TBI.
Method: 
 
The “Boolean logic” was used to search for articles on the subject matter in
PubMed and PubMed Central, as well as Google Scholar.
 
Results: 
Lithium’s therapeutic action is extremely complex, involving multiple effects
on gene secretion, neurotransmitter or receptor-mediated signaling, signal trans-
duction processes, circadian modulation, as well as ion transport. Lithium is able to
normalize multiple short- as well as long-term modifications in neuronal circuits that
ultimately result in disparity in cortical excitation and inhibition activated by TBI. Also,
lithium levels are more distinct in the hippocampus, thalamus, neo-cortex, olfactory
bulb, amygdala as well as the gray matter of the cerebellum following treatment of TBI.
 
Conclusion: 
Lithium attenuates neuroinflammation and neuronal toxicity as well as
protects the brain from edema, hippocampal neurodegeneration, loss of hemispheric
tissues, and enhanced memory as well as spatial learning after TBI.

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