Description

Celiac disease (CD) is an immune-mediated enteropathy triggered by the ingestion of gluten, a protein found in wheat, rye, and barley. With a global prevalence of approximately 1%, it is among the most common autoimmune disorders worldwide. Currently, the only accepted treatment is lifelong adherence to a strict gluten-free diet (GFD). It is now well recognized that CD is associated not only with varying degrees of small intestinal inflammation but also with a wide range of gastrointestinal and extraintestinal manifestations, and it may even be present in asymptomatic individuals. Common extraintestinal manifestations include abnormal liver enzymes, arthralgia/arthritis, alopecia, fatigue, headache, anemia, oral ulcers, myalgia, skin rashes, neuropathy, short stature, delayed puberty, osteoporosis, and infertility. The clinical diagnosis of CD is based on histological evaluation of small intestinal biopsies. Serological tests such as immunoglobulin A (IgA) anti-tissue transglutaminase antibodies and endomysial antibodies (EMA; IgA) may be useful in supporting the diagnosis. Several theories suggest that the globalization and spread of "incorrect" or "excessive" versions of the Mediterranean diet, characterized by very high gluten consumption (up to 20 g/day), may have contributed to the increasing prevalence and incidence of CD. In addition, gluten quality may also play a role. The production of new cereal variants for technological purposes in recent years may have influenced the observed rise in CD diagnoses. Except in regions with low frequencies of CD-predisposing genes and low gluten consumption (such as sub-Saharan Africa and Japan), CD prevalence is higher among first-degree relatives of affected individuals (10-15%) and in other high-risk groups, particularly patients with Down syndrome, type 1 diabetes, or IgA deficiency. In addition to genetic susceptibility and gluten exposure, loss of intestinal barrier function, gluten-triggered proinflammatory innate immune responses, inappropriate adaptive immune responses, and gut microbiome imbalance appear to constitute the fundamental components of CD autoimmunity. An abnormal immune response to gluten in CD classically leads to gastrointestinal symptoms such as abdominal pain, diarrhea, constipation, bloating, and weight loss. CD is now considered a multisystem disorder that affects not only the gastrointestinal tract but also the central nervous system, and has been associated with impairments in attention, short- and long-term memory, and executive function, commonly referred to as "brain fog." Dual-task (DT) gait is thought to involve higher-order cognitive processes that control and regulate behavior, including executive function, gait control, and attentional allocation. This process requires activation of multiple cortical regions, such as the prefrontal cortex (PFC), primary motor cortex, supplementary motor cortex, and somatosensory motor cortex. In addition to cortical activation, network efficiency and functional connectivity among various cortical regions, including the PFC and sensorimotor cortices, have been identified as important contributors to the cortical processes involved in DT gait. The aim of this study is to comprehensively investigate the effects of adherence to a gluten-free diet on cognitive, motor, and psychosocial functions in adolescents aged 8-18 years diagnosed with celiac disease. Accordingly, dual-task gait performance, cognitive processing speed and attentional functions, working memory and executive functions, muscle strength, quality of life, and fatigue levels of GFD-adherent and non-adherent individuals with CD will be compared with those of healthy peers. Furthermore, sleep patterns, pubertal development, socioeconomic indicators, and serological markers will be considered to evaluate the specific effects of dietary adherence on neurocognitive and functional outcomes.