Genetic variations and cognitive function in fibromyalgia
Selin Akdemir, Oznur Ozge Ozcan
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Introduction
Fibromyalgia (FM) is a chronic pain disorder characterized by widespread musculoskeletal pain, fatigue, sleep disturbances, cognitive impairments, and mood-related symptoms (Wolfe et al., 2016). The pathophysiology of FM is complex and involves genetic predispositions, neurobiological mechanisms, and environmental triggers that contribute to its manifestation (Siracusa et al., 2021).
While FM was historically classified as a rheumatologic condition, recent evidence suggests that it is primarily a central sensitization disorder, leading to altered pain processing in the central nervous system (Ibraheem et al., 2021). Genetic factors have been implicated in FM susceptibility, yet no single gene has been identified as solely responsible for the disorder (D’Agnelli et al., 2019). Additionally, individuals with FM frequently experience cognitive dysfunction, including memory lapses, impaired concentration, and slower mental processing, which significantly impact their quality of life (Galvez-Sánchez et al., 2018).
Understanding the genetic underpinnings of FM encompassing heritability, candidate genes, genome-wide association studies, and epigenetic modifications along with the mechanisms underlying cognitive impairments is crucial for advancing knowledge of the disorder.
This paper explores the current evidence on genetic contributions to FM and cognitive dysfunction. Furthermore, it examines potential interactions between genetic factors and cognitive symptoms, providing insights into future research directions and implications for patient care.
Web | PDF | Chapter: Health & Science 2025-III | Open Access
Selin Akdemir, Oznur Ozge Ozcan
[Line breaks added]
Introduction
Fibromyalgia (FM) is a chronic pain disorder characterized by widespread musculoskeletal pain, fatigue, sleep disturbances, cognitive impairments, and mood-related symptoms (Wolfe et al., 2016). The pathophysiology of FM is complex and involves genetic predispositions, neurobiological mechanisms, and environmental triggers that contribute to its manifestation (Siracusa et al., 2021).
While FM was historically classified as a rheumatologic condition, recent evidence suggests that it is primarily a central sensitization disorder, leading to altered pain processing in the central nervous system (Ibraheem et al., 2021). Genetic factors have been implicated in FM susceptibility, yet no single gene has been identified as solely responsible for the disorder (D’Agnelli et al., 2019). Additionally, individuals with FM frequently experience cognitive dysfunction, including memory lapses, impaired concentration, and slower mental processing, which significantly impact their quality of life (Galvez-Sánchez et al., 2018).
Understanding the genetic underpinnings of FM encompassing heritability, candidate genes, genome-wide association studies, and epigenetic modifications along with the mechanisms underlying cognitive impairments is crucial for advancing knowledge of the disorder.
This paper explores the current evidence on genetic contributions to FM and cognitive dysfunction. Furthermore, it examines potential interactions between genetic factors and cognitive symptoms, providing insights into future research directions and implications for patient care.
Web | PDF | Chapter: Health & Science 2025-III | Open Access