Authors :
Pasmas Coffie; Moses Mayonu; Onuh Matthew Ijiga; Idoko David Oche
Volume/Issue :
Volume 11 - 2026, Issue 5 - May
Google Scholar :
https://tinyurl.com/5fysch94
Scribd :
https://tinyurl.com/ycymwt8a
DOI :
https://doi.org/10.38124/ijisrt/26May1806
Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.
Abstract :
Psychosocial stress is increasingly recognized as a critical modifier of neurodegenerative disease progression, yet
its molecular underpinnings in African populations remain underexplored. This study investigates the relationship between
chronic stress exposure and epigenetic modifications associated with neurodegeneration among individuals living with type
2 diabetes. Using a cohort derived from outpatient clinics in Kumasi, Ghana, participants were assessed for perceived stress,
dietary patterns, and clinical biomarkers including glycemic status and lipid profiles. Blood samples were analyzed to
identify DNA methylation patterns and histone modification markers linked to neuroinflammatory and neurodegenerative
pathways. Statistical modeling was performed to evaluate associations between stress indices and epigenetic alterations while
controlling for metabolic and demographic variables. Findings reveal that elevated psychosocial stress correlates with
distinct epigenetic signatures, particularly in genes associated with neuronal survival, inflammation, and metabolic
regulation. These modifications were more pronounced in individuals with poor glycemic control, suggesting a synergistic
interaction between metabolic dysfunction and stress-induced epigenetic regulation. The study highlights the role of stress
as a biologically embedded risk factor influencing neurodegenerative trajectories and underscores the need for integrated
clinical approaches that incorporate mental health, metabolic care, and molecular diagnostics. This work contributes to a
growing body of evidence supporting the inclusion of epigenetic biomarkers in understanding disease progression and
tailoring interventions in diverse populations.
Keywords :
Psychosocial Stress, Epigenetic Modifications, Type 2 Diabetes, Neurodegenerative Disease Progression, DNA Methylation.
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Psychosocial stress is increasingly recognized as a critical modifier of neurodegenerative disease progression, yet
its molecular underpinnings in African populations remain underexplored. This study investigates the relationship between
chronic stress exposure and epigenetic modifications associated with neurodegeneration among individuals living with type
2 diabetes. Using a cohort derived from outpatient clinics in Kumasi, Ghana, participants were assessed for perceived stress,
dietary patterns, and clinical biomarkers including glycemic status and lipid profiles. Blood samples were analyzed to
identify DNA methylation patterns and histone modification markers linked to neuroinflammatory and neurodegenerative
pathways. Statistical modeling was performed to evaluate associations between stress indices and epigenetic alterations while
controlling for metabolic and demographic variables. Findings reveal that elevated psychosocial stress correlates with
distinct epigenetic signatures, particularly in genes associated with neuronal survival, inflammation, and metabolic
regulation. These modifications were more pronounced in individuals with poor glycemic control, suggesting a synergistic
interaction between metabolic dysfunction and stress-induced epigenetic regulation. The study highlights the role of stress
as a biologically embedded risk factor influencing neurodegenerative trajectories and underscores the need for integrated
clinical approaches that incorporate mental health, metabolic care, and molecular diagnostics. This work contributes to a
growing body of evidence supporting the inclusion of epigenetic biomarkers in understanding disease progression and
tailoring interventions in diverse populations.
Keywords :
Psychosocial Stress, Epigenetic Modifications, Type 2 Diabetes, Neurodegenerative Disease Progression, DNA Methylation.