Memory for forgetting in adults with persistent symptoms following concussion

Rioux, Mathilde; Wardell, Victoria; Palombo, Daniela J.; Picon, Edwina L; Le, M Lindy; Silverberg, Noah D.

doi:10.1080/13803395.2022.2067326

Cited by 9 publications

(4 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We next investigated the effects of SB332235 on behavioral phenotypes of the TBI mouse model, focusing on motor and memory performance, which are hallmarks of TBI in humans [ 27 , 30 ]. Beam-balance and beam-walk tests were used to evaluate gross and fine motor functions.…”

Section: Resultsmentioning

confidence: 99%

Neuroprotective Effects of CXCR2 Antagonist SB332235 on Traumatic Brain Injury Through Suppressing NLRP3 Inflammasome

Zhao,

Zhou,

Chen

et al. 2023

Neurochem Res

View full text Add to dashboard Cite

The inflammatory process mediated by nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain comprising 3 (NLRP3) inflammasome plays a predominant role in the neurological dysfunction following traumatic brain injury (TBI). SB332235, a highly selective antagonist of chemokine receptor 2 (CXCR2), has been demonstrated to exhibit anti-inflammatory properties and improve neurological outcomes in the central nervous system. We aimed to determine the neuroprotective effects of SB332235 in the acute phase after TBI in mice and to elucidate its underlying mechanisms. Male C57BL/6J animals were exposed to a controlled cortical impact, then received 4 doses of SB332235, with the first dose administered at 30 min after TBI, followed by additional doses at 6, 24, and 30 h. Neurological defects were assessed by the modified neurological severity score, while the motor function was evaluated using the beam balance and open field tests. Cognitive performance was evaluated using the novel object recognition test. Brain tissues were collected for pathological, Western blot, and immunohistochemical analyses. The results showed that SB332235 significantly ameliorated TBI-induced deficits, including motor and cognitive impairments. SB332235 administration suppressed expression of both CXCL1 and CXCR2 in TBI. Moreover, SB332235 substantially mitigated the augmented expression levels and activation of the NLRP3 inflammasome within the peri-contusional cortex induced by TBI. This was accompanied by the blocking of subsequent production of pro-inflammatory cytokines. Additionally, SB332235 hindered microglial activity induced by TBI. These findings confirmed the neuroprotective effects of SB332235 against TBI, and the involved mechanisms were in part due to the suppression of NLRP3 inflammasome activity. This study suggests that SB332235 may act as an anti-inflammatory agent to improve functional outcomes in brain injury when applied clinically.

show abstract

Section: Resultsmentioning

confidence: 99%

Neuroprotective Effects of CXCR2 Antagonist SB332235 on Traumatic Brain Injury Through Suppressing NLRP3 Inflammasome

Zhao,

Zhou,

Chen

et al. 2023

Neurochem Res

View full text Add to dashboard Cite

show abstract

“…We next investigated the effects of SB332235 on behavioral phenotypes of the TBI mouse model, focusing on motor and memory performance, which are hallmarks of TBI in humans [26,29]. Beambalance and beam-walk tests were used to evaluate gross and ne motor functions.…”

Section: Sb332235 Ameliorates Tbi-induced Behavioral De Citsmentioning

confidence: 99%

Neuroprotective Effects of CXCR2 Antagonist SB332235 on Traumatic Brain Injury Through Suppressing NLRP3 Inflammasome

Zhao

Zhou

Gou

et al. 2023

Preprint

View full text Add to dashboard Cite

The inflammatory process mediated by nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain comprising 3 (NLRP3) inflammasome plays a predominant role in the neurological dysfunction following traumatic brain injury (TBI). SB332235, a highly selective antagonist of chemokine receptor 2 (CXCR2), has been demonstrated to exhibit anti-inflammatory properties and improve neurological outcomes in the central nervous system. We aimed to determine the neuroprotective effects of SB332235 in the acute phase after TBI in mice and to elucidate its underlying mechanisms. Male C57BL/6J animals were exposed to a controlled cortical impact, then received 4 doses of SB332235, with the first dose administered 30 min after TBI, followed by additional doses at 6, 24, and 30 hours. Neurological defects were assessed by the modified neurological severity score, while the motor function was evaluated using the beam balance and open field tests. Cognitive performance was evaluated using the novel object recognition test. Brain tissues were collected for pathological, Western blot, and immunohistochemical analyses. The results showed that SB332235 significantly ameliorated TBI-induced deficits, including motor and cognitive impairments. Moreover, SB332235 substantially mitigated the augmented expression levels and activation of the NLRP3 inflammasome within the peri-contusional cortex induced by TBI. This was accompanied by the blocking of subsequent production of pro-inflammatory cytokines. Additionally, SB332235 hindered microglial activity induced by TBI. These findings confirmed the neuroprotective effects of SB332235 against TBI, and the involved mechanisms were in part due to the suppression of NLRP3 inflammasome activity. This study suggests that SB332235 may act as an anti-inflammatory agent to improve functional outcomes in brain injury when applied clinically.

show abstract

“…Only a few studies have pointed to episodic memory impairments in adults after mTBI ( Wammes et al, 2017 ; Fortier-Lebel et al, 2021 ) and recent studies concluded that memory complaints may not be associated with performance in memory tests after mTBI ( Anderson, 2021 ; Rioux et al, 2022 ). Similarly, parents of children who have sustained mTBI report memory problems ( Waldmeier-Wilhelm et al, 2019 ), although studies rarely report the performance of specific neuropsychological testing to identify episodic memory impairments ( Chadwick et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Impaired episodic verbal memory recall after 1 week and elevated forgetting in children after mild traumatic brain injury – results from a short-term longitudinal study

Lidzba,

Afridi,

Romano

et al. 2024

Front. Psychol.

View full text Add to dashboard Cite

ObjectiveThere is preliminary evidence that children after traumatic brain injury (TBI) have accelerated long-term forgetting (ALF), i.e., an adequate learning and memory performance in standardized memory tests, but an excessive rate of forgetting over delays of days or weeks. The main aim of this study was to investigate episodic memory performance, including delayed retrieval 1 week after learning, in children after mild TBI (mTBI).MethodsThis prospective study with two time-points (T1: 1 week after injury and T2: 3–6 months after injury), included data of 64 children after mTBI and 57 healthy control children aged between 8 and 16 years. We assessed episodic learning and memory using an auditory word learning test and compared executive functions (interference control, working memory, semantic fluency and flexibility) and divided attention between groups. We explored correlations between memory performance and executive functions. Furthermore, we examined predictive factors for delayed memory retrieval 1 week after learning as well as for forgetting over time.ResultsCompared to healthy controls, patients showed an impaired delayed recall and recognition performance 3–6 months after injury. Executive functions, but not divided attention, were reduced in children after mTBI. Furthermore, parents rated episodic memory as impaired 3–6 months after injury. Additionally, verbal learning and group, but not executive functions, were predictive for delayed recall performance at both time-points, whereas forgetting was predicted by group.DiscussionDelayed recall and forgetting over time were significantly different between groups, both post-acutely and in the chronic phase after pediatric mTBI, even in a very mildly injured patient sample. Delayed memory performance should be included in clinical evaluations of episodic memory and further research is needed to understand the mechanisms of ALF.

show abstract

Memory for forgetting in adults with persistent symptoms following concussion

Cited by 9 publications

References 55 publications

Neuroprotective Effects of CXCR2 Antagonist SB332235 on Traumatic Brain Injury Through Suppressing NLRP3 Inflammasome

Neuroprotective Effects of CXCR2 Antagonist SB332235 on Traumatic Brain Injury Through Suppressing NLRP3 Inflammasome

Neuroprotective Effects of CXCR2 Antagonist SB332235 on Traumatic Brain Injury Through Suppressing NLRP3 Inflammasome

Impaired episodic verbal memory recall after 1 week and elevated forgetting in children after mild traumatic brain injury – results from a short-term longitudinal study

Contact Info

Product

Resources

About