← Back to OverviewNeurotrition Research Lab

Clinical Focus

Subclinical Indications

Neurotrition targets three neurobiologically defined subclinical states — each representing a validated intervention window before irreversible clinical progression.

Indication I · MCI

Mild Cognitive Impairment

~20% prevalence

The prodromal stage between normal age-related cognitive change and diagnosable Alzheimer's disease — characterized by objective cognitive decline without functional impairment. The largest undertreated pre-clinical window before irreversible neurodegeneration.

Neurobiological Mechanisms

  • 01Cholinergic system hypofunction — reduced ACh synthesis and vesicular release from basal forebrain nuclei
  • 02Amyloid-β oligomer accumulation disrupting synaptic plasticity prior to plaque formation
  • 03Hippocampal atrophy and default mode network disconnection measurable by fMRI
  • 04Mitochondrial energy deficit in neurons — ATP insufficiency driving synaptic failure
  • 05Subclinical neuroinflammation — microglial priming elevating IL-1β, TNF-α without full activation

Assessment & Biomarkers

  • MoCA / MMSE score 24–27 (subclinical threshold)
  • EEG theta/alpha power ratio (hippocampal slowing)
  • fMRI: reduced DMN connectivity & hippocampal volume
  • Blood: BDNF, GFAP, neurofilament light chain (NfL)
  • Neuropsychological battery: episodic memory, processing speed
Neurotrition Intervention Approach

Cholinergic precursor supply, neurotrophic upregulation through NGF/BDNF activity, mitochondrial functionality restoration, phospholipid synthesis, thyroid support, and anti-neuroinflammatory support.

Indication II · CFS / ME

Chronic Fatigue Syndrome

2× increase post-pandemic

A neurobiologically measurable syndrome of persistent fatigue, cognitive impairment ('brain fog'), and autonomic dysregulation following viral insult. Characterized by mitochondrial dysfunction, immune dysregulation, and CNS hypometabolism — with no approved pharmacological treatment.

Neurobiological Mechanisms

  • 01Mitochondrial dysfunction — impaired complex I/III activity reducing neuronal ATP synthesis
  • 02Persistent neuroinflammation — activated microglia and elevated cytokine burden (IFN-γ, IL-6)
  • 03HPA-axis hypoactivity — flattened cortisol awakening response disrupting circadian rhythm
  • 04Autonomic nervous system imbalance — reduced HRV, sympathetic overdrive
  • 05Oxidative stress accumulation — depleted glutathione and antioxidant enzyme deficiency

Assessment & Biomarkers

  • Fatigue Severity Scale (FSS ≥ 36) & Chalder Fatigue Scale
  • Cortisol Awakening Response (CAR) — blunted morning cortisol
  • Heart Rate Variability (HRV) — resting RMSSD reduction
  • Blood: NK cell cytotoxicity, IL-6, IFN-γ, mitochondrial ROS
  • EEG: increased slow-wave activity, reduced cognitive event-related potentials
Neurotrition Intervention Approach

Mitochondrial electron chain restoration as well as ATP synthesis, acetylcholine synthesis, anti-neuroinflammatory effects, HPA-axis normalisation, circadian rhythm support, and antioxidant network restoration.

Indication III · BRN

Burnout

+84% sick days past decade

Chronic occupational stress-induced neurobiological deterioration — beyond psychological exhaustion. Measurable structural changes in prefrontal cortex and hippocampus, dopaminergic pathway exhaustion, and sustained HPA-axis dysregulation precede and outlast subjective burnout resolution.

Neurobiological Mechanisms

  • 01HPA-axis dysregulation — cortisol hypersecretion followed by adrenal hyporesponsiveness
  • 02Glucocorticoid-induced hippocampal atrophy — stress hormone excess drives dendritic retraction
  • 03Prefrontal hypoactivation — dopaminergic and noradrenergic depletion reducing executive function
  • 04Neuroinflammatory sensitisation — stress-primed microglia lowering the inflammatory threshold
  • 05Catecholamine precursor depletion — tyrosine availability limits dopamine synthesis

Assessment & Biomarkers

  • Maslach Burnout Inventory (MBI) — emotional exhaustion subscale
  • Cortisol Awakening Response + diurnal cortisol slope (saliva)
  • fMRI: prefrontal activation during working memory & amygdala reactivity
  • Blood: ACTH, catecholamine metabolites (HVA, MHPG), IL-6
  • HRV: resting parasympathetic tone as autonomic recovery marker
Neurotrition Intervention Approach

Catecholaminergic precursor restoration, HPA-axis normalisation, increase of neuroplasticity including phospholipid synthesis, neuroprotection against glucocorticoid neurotoxicity, and prefrontal circuit support.

View our Research Design →