» Articles » PMID: 28500417

Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury

Overview
Specialty Neurology
Date 2017 May 14
PMID 28500417
Citations 44
Authors
Affiliations
Soon will be listed here.
Abstract

Memory is fundamental to everyday life, and cognitive impairments resulting from traumatic brain injury (TBI) have devastating effects on TBI survivors. A contributing component to memory impairments caused by TBI is alteration in the neural circuits associated with memory function. In this review, we aim to bring together experimental findings that characterize behavioral memory deficits and the underlying pathophysiology of memory-involved circuits after TBI. While there is little doubt that TBI causes memory and cognitive dysfunction, it is difficult to conclude which memory phase, i.e., encoding, maintenance, or retrieval, is specifically altered by TBI. This is most likely due to variation in behavioral protocols and experimental models. Additionally, we review a selection of experimental treatments that hold translational potential to mitigate memory dysfunction following injury.

Citing Articles

Neurological manifestations of encephalitic alphaviruses, traumatic brain injuries, and organophosphorus nerve agent exposure.

VanderGiessen M, de Jager C, Leighton J, Xie H, Theus M, Johnson E Front Neurosci. 2024; 18:1514940.

PMID: 39734493 PMC: 11671522. DOI: 10.3389/fnins.2024.1514940.


Verbal Learning and Memory Deficits across Neurological and Neuropsychiatric Disorders: Insights from an ENIGMA Mega Analysis.

Kennedy E, Liebel S, Lindsey H, Vadlamani S, Lei P, Adamson M Brain Sci. 2024; 14(7).

PMID: 39061410 PMC: 11274572. DOI: 10.3390/brainsci14070669.


Single Nucleotide Polymorphism in Cell Adhesion Molecule L1 Affects Learning and Memory in a Mouse Model of Traumatic Brain Injury.

Jiang H, Giarratana A, Theis T, Nagaraj V, Zhou X, Thakker-Varia S Int J Mol Sci. 2024; 25(5).

PMID: 38474289 PMC: 10932301. DOI: 10.3390/ijms25053043.


Nicorandil attenuates cognitive impairment after traumatic brain injury via inhibiting oxidative stress and inflammation: Involvement of BDNF and NGF.

Tu Y, Han D, Liu Y, Hong D, Chen R Brain Behav. 2024; 14(1):e3356.

PMID: 38376046 PMC: 10757892. DOI: 10.1002/brb3.3356.


Overexpress miR-132 in the Brain Parenchyma by a Non-invasive Way Improves Tissue Repairment and Releases Memory Impairment After Traumatic Brain Injury.

Jia M, Guo X, Liu R, Sun L, Wang Q, Wu J Cell Mol Neurobiol. 2023; 44(1):5.

PMID: 38104297 PMC: 11397820. DOI: 10.1007/s10571-023-01435-4.


References
1.
Sebastian V, Diallo A, Ling D, Serrano P . Robust training attenuates TBI-induced deficits in reference and working memory on the radial 8-arm maze. Front Behav Neurosci. 2013; 7:38. PMC: 3642509. DOI: 10.3389/fnbeh.2013.00038. View

2.
Gao J, Prough D, McAdoo D, Grady J, Parsley M, Ma L . Transplantation of primed human fetal neural stem cells improves cognitive function in rats after traumatic brain injury. Exp Neurol. 2006; 201(2):281-92. DOI: 10.1016/j.expneurol.2006.04.039. View

3.
Fox G, Fan L, LeVasseur R, Faden A . Effect of traumatic brain injury on mouse spatial and nonspatial learning in the Barnes circular maze. J Neurotrauma. 1999; 15(12):1037-46. DOI: 10.1089/neu.1998.15.1037. View

4.
Johnson B, Palmer C, Bourgeois E, Elkind J, Putnam B, Cohen A . Augmented Inhibition from Cannabinoid-Sensitive Interneurons Diminishes CA1 Output after Traumatic Brain Injury. Front Cell Neurosci. 2015; 8:435. PMC: 4271495. DOI: 10.3389/fncel.2014.00435. View

5.
Schiff N, Giacino J, Kalmar K, Victor J, Baker K, Gerber M . Behavioural improvements with thalamic stimulation after severe traumatic brain injury. Nature. 2007; 448(7153):600-3. DOI: 10.1038/nature06041. View