As the global population ages, the incidence of sarcopenia—a progressive loss of muscle mass and strength—poses a mounting challenge to healthcare systems worldwide. New research emerging from India reveals compelling biochemical links between neurodegenerative markers and sarcopenia, potentially opening avenues for earlier diagnosis and intervention strategies. In a groundbreaking study led by Rao, Bhagwasia, Anwar, and colleagues, scientists explored the association between neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), and sarcopenia among older Indian adults. Drawing from comprehensive data within the Longitudinal Aging Study in India–Diagnostic Assessment of Dementia (LASI-DAD), their findings published in BMC Geriatrics underscore intricate neuro-muscular interactions that transcend traditional boundaries of geriatric medicine.
Sarcopenia, widely recognized as a debilitating condition characterized by the gradual degradation of skeletal muscle tissue, significantly impacts quality of life and functional independence in the elderly. Until now, the molecular underpinnings connecting neurodegeneration and muscular atrophy remained elusive, particularly within South Asian populations. This pioneering investigation into circulating biomarkers potentially bridges this gap by implicating central nervous system damage markers as significant correlates of sarcopenia severity. Notably, the study focuses on two proteins, neurofilament light chain and GFAP, both integral components of neural integrity and reactive gliosis respectively, whose elevated levels in peripheral blood may mirror ongoing neurodegenerative processes.
Neurofilament light chain (NfL) is a structural protein prevalent in axons, released into bodily fluids upon neuronal injury. Its utility as a biomarker has been well-documented across neurodegenerative disorders such as Alzheimer’s disease and multiple sclerosis. In this Indian cohort, NfL levels were measured against sarcopenic indices including muscle mass and grip strength, revealing a robust positive association between increased NfL and heightened sarcopenic burden. This suggests that neuroaxonal damage may parallel or perhaps even precipitate muscular degeneration, underscoring a shared pathological axis involving both the nervous and musculoskeletal systems with age-related decline.
Likewise, glial fibrillary acidic protein (GFAP), an intermediate filament protein expressed by astrocytes, serves as a sensitive marker for astroglial activation and central nervous system injury. Elevated peripheral concentrations of GFAP in individuals diagnosed with sarcopenia highlight a potential neuroinflammatory component entwined with muscle deterioration. The researchers postulate that reactive astrogliosis—evidenced by GFAP expression—may contribute to neurogenic mechanisms accelerating muscular atrophy, suggesting a broader systemic milieu of age-related neuroinflammation that permeates beyond neuronal damage alone.
The investigation drew data from LASI-DAD, a large-scale, nationally representative study designed to evaluate neurocognitive health among older Indian adults. By integrating biochemical assays with extensive geriatric assessments, the team could elucidate statistically significant links while controlling for confounding variables such as comorbidities, lifestyle factors, and socioeconomic status. The rigorous methodological framework bolstered the credibility of their conclusions and positioned this study as a defining contribution to the understanding of aging physiology in a globally underrepresented demographic.
This novel research demands reconsideration of how clinicians approach sarcopenia management. The findings propose that assessment of neurodegenerative biomarkers could enhance prognostic accuracy, enabling personalized intervention paradigms that address both neurological and muscular deterioration. Moreover, the bidirectional interplay suggested between the nervous system and muscle health could spur development of therapeutics targeting neuroinflammation pathways alongside conventional muscle-strengthening strategies.
Mechanistically, the study sheds light on the potential molecular pathways linking neurodegeneration and sarcopenia. Impaired axonal integrity, reflected by elevated NfL, may disrupt motor neuron function critical for muscle innervation. Meanwhile, GFAP elevation points to astrocytic activation which can catalyze chronic inflammatory states detrimental to neuronal survival and muscle trophism. These insights align with emerging paradigm shifts recognizing sarcopenia not merely as a muscular disorder but as a complex systemic condition influenced by neuroimmune interactions.
From a public health standpoint, awareness of such biomarker associations could revolutionize aging care management in India and similar settings. With aging populations burgeoning, early identification of individuals at risk for both cognitive decline and sarcopenia through minimally invasive blood tests could facilitate timely therapeutic interventions and reduce healthcare burden caused by falls, frailty, and dependency. This is particularly critical in low-resource environments where advanced imaging or neurological testing may be less accessible.
The study’s implications extend beyond diagnostic utility. It opens promising research pathways investigating whether modulating neuroinflammation or protecting neuronal integrity could mitigate sarcopenic progression. Interdisciplinary collaborations examining the interface of neurology, geriatrics, and muscle biology are poised to transform our holistic understanding of aging and inform novel therapeutic development.
Future work inspired by these findings should also explore how genetic factors, environmental influences, and metabolic dysfunction intersect with neurodegenerative markers to influence sarcopenia risk. Longitudinal follow-ups from LASI-DAD could clarify causality, track disease trajectories, and evaluate potential reversibility through targeted interventions addressing the nervous system-muscle axis.
Importantly, the study underscores the value of diverse population-based studies in unearthing universal versus population-specific aging mechanisms. India’s unique demographic and epidemiological landscape provided fertile ground for such revelations, emphasizing the necessity of inclusive research paradigms that inform global aging challenges.
The comprehensive assessment of NfL and GFAP within this geriatric population also sets a benchmark for future biomarker-driven investigations. In turn, this approach may enable stratification of sarcopenia phenotypes, assisting clinicians in tailoring treatment regimes according to individual biomarker profiles rather than relying solely on clinical symptomatology.
In conclusion, Rao, Bhagwasia, Anwar, and their team’s work convincingly demonstrates that neurofilament light chain and glial fibrillary acidic protein are significantly correlated with sarcopenia in older Indian adults. Their findings establish a critical molecular nexus between neurodegeneration and muscle aging—a nexus that heralds a new frontier in geriatric medicine. This pioneering study not only enriches scientific discourse but also kindles hope for innovative diagnostic and therapeutic strategies to alleviate the burden of sarcopenia and enhance the healthspan of aging populations worldwide.
Subject of Research:
Association of neurodegenerative biomarkers with sarcopenia in elderly Indian adults.
Article Title:
Association between neurofilament light chain, glial fibrillary acidic protein, and sarcopenia in older Indian adults: evidence from LASI-DAD.
Article References:
Rao, A.R., Bhagwasia, M., Anwar, M. et al. Association between neurofilament light chain, glial fibrillary acidic protein, and sarcopenia in older Indian adults: evidence from LASI-DAD. BMC Geriatr (2026). https://doi.org/10.1186/s12877-026-07151-0
Image Credits: AI Generated
DOI: 10.1186/s12877-026-07151-0
Keywords:
Neurofilament light chain, glial fibrillary acidic protein, sarcopenia, neurodegeneration, aging, muscle atrophy, biomarkers, neuroinflammation, elderly, India, LASI-DAD
