What question did this study set out to answer?

To determine how neuropathologic Alzheimer's disease diagnosis and APOE4 status impact the human skeletal muscle proteome across different muscle types.

April 16, 2025Neurobiology of DiseaseOpen Access

Human skeletal muscle mitochondrial pathways are impacted by a neuropathologic diagnosis of Alzheimer's disease

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Authors

CJChelsea N. JohnsonUniversity of Kansas ABAnneka E. BlankenshipUniversity of Kansas Medical Center CJCasey S. JohnAlzheimer’s Disease Neuroimaging Initiative

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Overview

Cross-sectional proteomic analysis reveals downregulated mitochondrial pathways in skeletal muscle of Alzheimer's disease patients, suggesting systemic metabolic impairment amplified by APOE4.

Key Points

To determine how neuropathologic Alzheimer's disease diagnosis and APOE4 status impact the human skeletal muscle proteome across different muscle types.
Analyzed the proteome of human quadriceps (n = 81) and temporalis (n = 66) muscle tissues stratified by Alzheimer's Disease Neuropathologic Change status (ADNPC+: n = 54 temporalis, 44 quadriceps; ADNPC-: n = 27 temporalis, 22 quadriceps).
Assessed differential protein expression within each muscle type and across apolipoprotein E4 (APOE4) carrier and non-carrier groups.
Correlated altered oxidative phosphorylation protein levels with Alzheimer's disease progression using Clinical Dementia Rating and ADNPC scores.
Mitochondrial metabolism pathways, particularly oxidative phosphorylation, were significantly downregulated in skeletal muscle of ADNPC+ compared to ADNPC- individuals.
Mitochondrial proteomic alterations were most pronounced in APOE4 carriers, and temporalis muscle exhibited nearly four times more altered proteins than quadriceps tissue.
Expression of ~29% to 61% of oxidative phosphorylation proteins correlated with disease progression, with 23 proteins consistently declining across all muscle types and APOE4 groups.

Cite This Study

Johnson et al. (2025) studied this question.

synapsesocial.com/papers/6a9e5da651ef4ef99f055f9d https://doi.org/10.1016/j.nbd.2025.106916

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April 16, 2025Neurobiology of DiseaseOpen Access

Human skeletal muscle mitochondrial pathways are impacted by a neuropathologic diagnosis of Alzheimer's disease

View Full Paper

Ask AI

Bookmark

Authors

CJChelsea N. JohnsonUniversity of Kansas ABAnneka E. BlankenshipUniversity of Kansas Medical Center CJCasey S. JohnAlzheimer’s Disease Neuroimaging Initiative

Discussion

Member takes

Overview

Cross-sectional proteomic analysis reveals downregulated mitochondrial pathways in skeletal muscle of Alzheimer's disease patients, suggesting systemic metabolic impairment amplified by APOE4.

Key Points

To determine how neuropathologic Alzheimer's disease diagnosis and APOE4 status impact the human skeletal muscle proteome across different muscle types.
Analyzed the proteome of human quadriceps (n = 81) and temporalis (n = 66) muscle tissues stratified by Alzheimer's Disease Neuropathologic Change status (ADNPC+: n = 54 temporalis, 44 quadriceps; ADNPC-: n = 27 temporalis, 22 quadriceps).
Assessed differential protein expression within each muscle type and across apolipoprotein E4 (APOE4) carrier and non-carrier groups.
Correlated altered oxidative phosphorylation protein levels with Alzheimer's disease progression using Clinical Dementia Rating and ADNPC scores.
Mitochondrial metabolism pathways, particularly oxidative phosphorylation, were significantly downregulated in skeletal muscle of ADNPC+ compared to ADNPC- individuals.
Mitochondrial proteomic alterations were most pronounced in APOE4 carriers, and temporalis muscle exhibited nearly four times more altered proteins than quadriceps tissue.
Expression of ~29% to 61% of oxidative phosphorylation proteins correlated with disease progression, with 23 proteins consistently declining across all muscle types and APOE4 groups.

Cite This Study

Johnson et al. (2025) studied this question.

synapsesocial.com/papers/6a9e5da651ef4ef99f055f9d https://doi.org/10.1016/j.nbd.2025.106916

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