Elamipretide (SS-31) and Nicotinamide Mononucleotide (NMN) Combination Therapy Targets TREM2 to Mitigate Post-ischemic Brain Injury in Mice.

Yang Q, Zhang Y, Liu P, Yan Z, Li C, Tang Y, Yang Q

Neurochemical research14 Jul 2026

PMID42443448DOI10.1007/s11064-026-04846-zPepBankPUB-42443448

Publisher page PubMedAsk about this study

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study23

2 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Efficacy outcome
In mice with ischemic stroke, SS-31 plus NMN reduced brain damage more than SS-31 alone.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN reduced brain damage more than SS-31 alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreasePost-ischemic brain damage
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Comparator
SS-31 monotherapy
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Co-administration of SS-31 and NMN significantly attenuated post-ischemic brain damage and ameliorated neurological deficits (P < 0.0001), demonstrating effects markedly superior to either monotherapy.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
Report a problemFND-4244344810
02AnimalAnimal study (in vivo)Efficacy outcome
In mice with ischemic stroke, SS-31 plus NMN reduced neurological deficits more than SS-31 alone.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN reduced neurological deficits more than SS-31 alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseNeurological deficits
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Comparator
SS-31 monotherapy
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Co-administration of SS-31 and NMN significantly attenuated post-ischemic brain damage and ameliorated neurological deficits (P < 0.0001), demonstrating effects markedly superior to either monotherapy.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
Report a problemFND-4244344812

Studies that did not test the peptide alone21

In this study, the peptide was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking the peptide.

03AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Efficacy outcome
In mice with ischemic stroke, combined SS‑31 and NMN attenuated brain damage more than either monotherapy.
In plain wordsIn mice with stroke, SS‑31 given together with NMN reduced brain damage more than either one alone.
Peptide
Elamipretide (SS-31)
Outcome
DecreasePost-ischemic brain damage
Study
mousen: not reported in source
MCAO/R ischemic stroke model
Comparator
SS-31 or NMN alone
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Co-administration of SS-31 and NMN significantly attenuated post-ischemic brain damage and ameliorated neurological deficits (P < 0.0001), demonstrating effects markedly superior to either monotherapy.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Report a problemFND-4244344801
04AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Efficacy outcome
In mice with ischemic stroke, combined SS‑31 and NMN ameliorated neurological deficits (P < 0.0001), with effects superior to either monotherapy.
In plain wordsIn mice with stroke, SS‑31 given together with NMN improved movement and nerve function more than either one alone.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseNeurological deficits
Study
mousen: not reported in source
MCAO/R ischemic stroke model
Comparator
SS-31 or NMN alone
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Co-administration of SS-31 and NMN significantly attenuated post-ischemic brain damage and ameliorated neurological deficits (P < 0.0001), demonstrating effects markedly superior to either monotherapy.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Report a problemFND-4244344802
05AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, the SS‑31 and NMN combination downregulated TREM2.
In plain wordsIn mice with stroke, SS‑31 given together with NMN lowered TREM2, a protein linked to inflammation.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseTREM2 expression
Study
mousen: not reported in source
MCAO/R ischemic stroke model
Outcome group
Inflammation markers · Nervous system and cognition
Source sentences
Summary
Transcriptomic profiling revealed that the combination therapy specifically modulated innate immune and apoptotic pathways, concomitant with a significant downregulation of TREM2.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Report a problemFND-4244344803
06AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, the SS‑31 and NMN combination modulated innate immune and apoptotic pathways.
In plain wordsIn mice with stroke, SS‑31 given together with NMN changed immune and cell-death pathways.
Peptide
Elamipretide (SS-31)
Outcome
MixedInnate immune and apoptotic pathways
Study
mousen: not reported in source
MCAO/R ischemic stroke model
Outcome group
Inflammation markers · Nervous system and cognition
Source sentences
Summary
Transcriptomic profiling revealed that the combination therapy specifically modulated innate immune and apoptotic pathways, concomitant with a significant downregulation of TREM2.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Report a problemFND-4244344804
07AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, the SS‑31 and NMN combination inhibited NF-κB (p65) activation.
In plain wordsIn mice with stroke, SS‑31 given together with NMN reduced activation of the NF-κB inflammation pathway.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseNF-κB (p65) activation
Study
mousen: not reported in source
MCAO/R ischemic stroke model
Outcome group
Inflammation markers · Nervous system and cognition
Source sentences
Summary
Mechanistically, the combination therapy effectively inhibited NF-κB (p65) activation, thereby downregulating TREM2 expression.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Report a problemFND-4244344805
08AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, the SS‑31 and NMN combination attenuated microglial activation.
In plain wordsIn mice with stroke, SS‑31 given together with NMN reduced activation of immune cells in the brain.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseMicroglial activation
Study
mousen: not reported in source
MCAO/R ischemic stroke model
Outcome group
Inflammation markers · Nervous system and cognition
Source sentences
Summary
This suppression attenuated microglial activation, reduced the expression of canonical pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), and rebalanced the Bcl-2/Bax apoptotic axis.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Report a problemFND-4244344806
09AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, the SS‑31 and NMN combination reduced expression of IL-1β, TNF-α and IL-6.
In plain wordsIn mice with stroke, SS‑31 given together with NMN lowered inflammatory signal proteins.
Peptide
Elamipretide (SS-31)
Outcome
DecreasePro-inflammatory cytokines (IL-1β, TNF-α, IL-6)
Study
mousen: not reported in source
MCAO/R ischemic stroke model
Outcome group
Inflammation markers · Nervous system and cognition
Source sentences
Summary
This suppression attenuated microglial activation, reduced the expression of canonical pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), and rebalanced the Bcl-2/Bax apoptotic axis.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Report a problemFND-4244344807
10AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, the SS‑31 and NMN combination rebalanced the Bcl-2/Bax apoptotic axis.
In plain wordsIn mice with stroke, SS‑31 given together with NMN rebalanced proteins that control cell death.
Peptide
Elamipretide (SS-31)
Outcome
MixedBcl-2/Bax apoptotic axis
Study
mousen: not reported in source
MCAO/R ischemic stroke model
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
This suppression attenuated microglial activation, reduced the expression of canonical pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), and rebalanced the Bcl-2/Bax apoptotic axis.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Report a problemFND-4244344808
11AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, TREM2 overexpression entirely reversed the neuroprotective benefits of the SS‑31 and NMN combination.
In plain wordsIn mice with stroke, raising TREM2 fully undid the protective effects of SS‑31 given together with NMN.
Peptide
Elamipretide (SS-31)
Outcome
Not applicableEffect of TREM2 overexpression on combination benefit
Study
mousen: not reported in source
MCAO/R ischemic stroke model
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Overexpression of TREM2 entirely reversed these neuroprotective benefits.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).
Report a problemFND-4244344809
12AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice with ischemic stroke, SS-31 plus NMN reduced brain damage more than NMN alone.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN reduced brain damage more than NMN alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreasePost-ischemic brain damage
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Comparator
NMN monotherapy
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Co-administration of SS-31 and NMN significantly attenuated post-ischemic brain damage and ameliorated neurological deficits (P < 0.0001), demonstrating effects markedly superior to either monotherapy.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4244344811
13AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Efficacy outcome
In mice with ischemic stroke, SS-31 plus NMN reduced neurological deficits more than NMN alone.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN reduced neurological deficits more than NMN alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseNeurological deficits
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Comparator
NMN monotherapy
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Co-administration of SS-31 and NMN significantly attenuated post-ischemic brain damage and ameliorated neurological deficits (P < 0.0001), demonstrating effects markedly superior to either monotherapy.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4244344813
14AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, SS-31 plus NMN modulated innate immune pathways.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN changed innate immune pathways.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
Direction not reportedInnate immune pathways
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Outcome group
Immune response · Immune and inflammation
Source sentences
Summary
Transcriptomic profiling revealed that the combination therapy specifically modulated innate immune and apoptotic pathways, concomitant with a significant downregulation of TREM2.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4244344814
15AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, SS-31 plus NMN modulated apoptotic pathways.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN changed pathways involved in cell death.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
Direction not reportedApoptotic pathways
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Source sentences
Summary
Transcriptomic profiling revealed that the combination therapy specifically modulated innate immune and apoptotic pathways, concomitant with a significant downregulation of TREM2.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4244344815
16AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, SS-31 plus NMN downregulated TREM2 expression.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN reduced TREM2 expression.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseTREM2 expression
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Outcome group
Receptor activity and mechanism · Immune and inflammation
Source sentences
Summary
Mechanistically, the combination therapy effectively inhibited NF-κB (p65) activation, thereby downregulating TREM2 expression.
2 context sentences(design, population, supporting numbers)
Summary · context
Transcriptomic profiling revealed that the combination therapy specifically modulated innate immune and apoptotic pathways, concomitant with a significant downregulation of TREM2.
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4244344816
17AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, SS-31 plus NMN inhibited NF-κB (p65) activation.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN reduced activation of NF-κB.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseNF-κB (p65) activation
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Outcome group
Receptor activity and mechanism · Immune and inflammation
Source sentences
Summary
Mechanistically, the combination therapy effectively inhibited NF-κB (p65) activation, thereby downregulating TREM2 expression.
1 context sentence(design, population, supporting numbers)
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4244344817
18AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, suppression by SS-31 plus NMN attenuated microglial activation.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN reduced microglial activation.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseMicroglial activation
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Outcome group
Immune response · Immune and inflammation
Source sentences
Summary
This suppression attenuated microglial activation, reduced the expression of canonical pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), and rebalanced the Bcl-2/Bax apoptotic axis.
2 context sentences(design, population, supporting numbers)
Summary · context
Mechanistically, the combination therapy effectively inhibited NF-κB (p65) activation, thereby downregulating TREM2 expression.
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4244344818
19AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, suppression by SS-31 plus NMN reduced IL-1β expression.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN reduced IL-1β expression.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseIL-1β expression
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Outcome group
Inflammation markers · Immune and inflammation
Source sentences
Summary
This suppression attenuated microglial activation, reduced the expression of canonical pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), and rebalanced the Bcl-2/Bax apoptotic axis.
2 context sentences(design, population, supporting numbers)
Summary · context
Mechanistically, the combination therapy effectively inhibited NF-κB (p65) activation, thereby downregulating TREM2 expression.
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4244344819
20AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, suppression by SS-31 plus NMN reduced TNF-α expression.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN reduced TNF-α expression.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseTNF-α expression
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Outcome group
Inflammation markers · Immune and inflammation
Source sentences
Summary
This suppression attenuated microglial activation, reduced the expression of canonical pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), and rebalanced the Bcl-2/Bax apoptotic axis.
2 context sentences(design, population, supporting numbers)
Summary · context
Mechanistically, the combination therapy effectively inhibited NF-κB (p65) activation, thereby downregulating TREM2 expression.
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4244344820
21AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, suppression by SS-31 plus NMN reduced IL-6 expression.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN reduced IL-6 expression.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseIL-6 expression
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Outcome group
Inflammation markers · Immune and inflammation
Source sentences
Summary
This suppression attenuated microglial activation, reduced the expression of canonical pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), and rebalanced the Bcl-2/Bax apoptotic axis.
2 context sentences(design, population, supporting numbers)
Summary · context
Mechanistically, the combination therapy effectively inhibited NF-κB (p65) activation, thereby downregulating TREM2 expression.
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4244344821
22AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, suppression by SS-31 plus NMN rebalanced the Bcl-2/Bax apoptotic axis.
In plain wordsIn mice with ischemic stroke, SS-31 plus NMN rebalanced the Bcl-2/Bax cell death pathway.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
Direction not reportedBcl-2/Bax apoptotic axis
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Source sentences
Summary
This suppression attenuated microglial activation, reduced the expression of canonical pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), and rebalanced the Bcl-2/Bax apoptotic axis.
2 context sentences(design, population, supporting numbers)
Summary · context
Mechanistically, the combination therapy effectively inhibited NF-κB (p65) activation, thereby downregulating TREM2 expression.
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4244344822
23AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice with ischemic stroke, TREM2 overexpression entirely reversed the neuroprotective benefits of SS-31 plus NMN.
In plain wordsIn mice with ischemic stroke, TREM2 overexpression reversed the brain protection from SS-31 plus NMN.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseReversal of neuroprotection by TREM2 overexpression
Study
mousen: not reported in source
Male mice with middle cerebral artery occlusion/reperfusion
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Overexpression of TREM2 entirely reversed these neuroprotective benefits.
3 context sentences(design, population, supporting numbers)
Summary · context
Co-administration of SS-31 and NMN significantly attenuated post-ischemic brain damage and ameliorated neurological deficits (P < 0.0001), demonstrating effects markedly superior to either monotherapy.
Summary · context
TREM2 overexpression experiments and specific pharmacological inhibition of the NF-κB pathway were conducted to elucidate the specific molecular mechanisms.
Summary · context
A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male mice, followed by treatment with SS-31, NMN, or their combination.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4244344823

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Versions 4 to 12Current
28 Oct 2026, 02:02 UTC
The same notice was added 9 times, first on 21 Oct 2026, 15:59 UTC. The status did not change between them.
Study results updated
Version 3
21 Oct 2026, 12:50 UTC
Study data updated · source update from Europe PMC
Version 2
10 Oct 2026, 08:19 UTC
Study results updated
Version 1
9 Oct 2026, 02:47 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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Keywords

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