Routine serum biochemical analytes provide complementary information on nutritional and metabolic status in MND when interpreted alongside inflammatory markers and anthropometry, with serum creatinine emerging as a longitudinal marker of muscle wasting and lipid and retinol-binding protein alterations highlighting non-nutritional disease mechanisms that may confound standard biomarker interpretation.
Key Findings
Results
Low-grade systemic inflammation was present in nearly half of MND participants at enrolment, most commonly reflected by elevated fibrinogen.
9 out of 19 participants (47%) showed evidence of baseline inflammation at enrolment.
Elevated fibrinogen was the most common inflammatory marker identified.
Participants with baseline inflammation were excluded from nutritional biomarker analyses, yielding a non-inflammatory sub-cohort of n=10.
This high prevalence of inflammation underscores the importance of accounting for inflammatory status when interpreting nutritional biomarkers in MND.
Results
Serum creatinine was positively correlated with muscle-related functional subscores and declined significantly over the follow-up period in participants without inflammation.
Serum creatinine correlated positively with muscle-related functional subscores (p = 0.007) in the non-inflammatory sub-cohort (n=10).
Creatinine declined significantly between enrolment and three months (p = 0.02).
Creatinine showed predominantly negative trajectories by nine months of follow-up.
These findings position serum creatinine as a longitudinal marker of muscle wasting reflective of both denervation and nutritional depletion.
Results
HDL cholesterol declined over the nine-month follow-up period and lipid fractions correlated positively with disease stage, suggesting evolving metabolic stress.
HDL cholesterol declined significantly over the nine-month follow-up (p = 0.03) in the non-inflammatory sub-cohort.
Lipid fractions correlated positively with disease stage (p <0.001–0.02).
These lipid alterations were interpreted as reflecting non-nutritional disease mechanisms rather than purely dietary inadequacy.
The authors note that lipid changes may confound standard nutritional biomarker interpretation in MND.
Results
Elevated serum retinol-binding protein was observed in the large majority of participants without systemic inflammation.
Elevated serum retinol-binding protein was detected in 90% (9/10) of participants in the non-inflammatory sub-cohort.
The authors suggest this elevation reflects non-nutritional disease mechanisms rather than nutritional sufficiency.
Retinol-binding protein alterations are highlighted as a potential confounder of standard nutritional biomarker interpretation in MND.
This finding was consistent across the non-inflammatory sub-cohort regardless of disease severity.
Results
Biochemical evidence of malnutrition was detected in one-third of participants and was accompanied by weight loss and reductions in limb anthropometric parameters.
Low transferrin and/or creatinine indicating malnutrition was found in one-third of participants.
Malnutrition was accompanied by weight loss and reductions in limb anthropometric parameters.
Malnutrition risk was identified in 1/10 (10%) of the non-inflammatory sub-cohort using a modified ESPEN-based framework.
Using GLIM criteria, malnutrition risk was identified in 2/10 (20%) participants, demonstrating that the diagnostic framework used affects prevalence estimates.
Methods
The study followed 19 MND participants longitudinally using serum biomarkers, inflammatory markers, disease staging tools, and anthropometric measures at enrolment and three-month intervals up to nine months.
This was a single-centre, longitudinal prospective cohort study with 19 participants with confirmed MND.
Assessments occurred at enrolment and at three-month intervals up to nine months.
Serum analytes measured included albumin, prealbumin, creatinine, transferrin, ferritin, retinol-binding protein, and lipid fractions alongside routine inflammatory markers.
Disease severity and progression were assessed using the revised ALS functional rating scale (ALSFRS-R) and King's College Staging System.
Anthropometry included percentage weight change, BMI, mid-upper arm circumference, triceps skinfold thickness, arm muscle area, and calf circumference.
Conclusions
The authors conclude that a multimodal approach to nutritional monitoring in MND is warranted, emphasising that findings are hypothesis-generating due to small sample size and limited representation of non-ALS phenotypes.
The authors explicitly state findings 'should be regarded as hypothesis-generating and require confirmation in larger, multicentre cohorts with balanced phenotypic representation.'
Sample size was small (n=19 overall; n=10 non-inflammatory sub-cohort), limiting generalisability.
Non-ALS MND phenotypes were described as having limited representation in the cohort.
The study supports interpreting serum biomarkers alongside inflammatory markers and anthropometry rather than in isolation.
What This Means
This research suggests that standard blood tests used to assess nutrition in people with motor neuron disease (MND) need careful interpretation because the disease itself causes biological changes that can make these tests misleading. The study followed 19 people with MND over nine months, measuring blood proteins, fats, and inflammatory markers alongside physical measurements like arm and calf size. A key finding was that nearly half of participants showed signs of low-grade inflammation at the start of the study, which is known to distort nutritional blood test results — highlighting why inflammation must be checked before drawing conclusions from these markers.
Among participants without inflammation, the study found that a blood marker called creatinine — normally used to assess kidney function — actually tracked muscle wasting over time in MND, declining significantly within the first three months and continuing to fall. Levels of HDL cholesterol (often called 'good' cholesterol) also fell over nine months, and fat-related blood markers shifted in ways that appeared linked to disease progression rather than diet alone. Notably, a protein called retinol-binding protein was elevated in 90% of participants without inflammation, even though high levels are typically interpreted as a sign of good nutritional status — suggesting the disease process itself was driving this result rather than adequate nutrition.
This research suggests that no single blood test can reliably capture nutritional status in MND on its own. Instead, a combination of blood biomarkers, inflammation markers, and physical measurements is needed to build an accurate picture. The authors are careful to note that because the study involved only 19 participants at a single centre, these findings should be seen as preliminary and need to be confirmed in larger studies before clinical practice is changed.
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Roscoe S, Allen S, McDermott C, Stavroulakis T. (2026). Serum Biomarkers for Nutritional Monitoring in Motor Neuron Disease: A Longitudinal Cohort Study.. Nutrients. https://doi.org/10.3390/nu18172913