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Research Focus

Research Focus Areas

Our research programme addresses three subclinical states, each defined by neurobiological markers described in the published literature. The sections below summarise that literature on the conditions themselves — they are the starting point for our studies, not a description of product effects.

Focus Area I · MCI

Mild Cognitive Impairment

~20% age 65+

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
Mechanistic Hypotheses Under Investigation

Our research programme investigates for example whether cholinergic precursor availability, NGF/BDNF signalling, mitochondrial function, phospholipid synthesis, thyroid-related metabolism and inflammatory markers are relevant nutritional targets in this state.

Focus Area 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
Mechanistic Hypotheses Under Investigation

Our research programme investigates for example whether mitochondrial electron chain function, ATP and acetylcholine synthesis, inflammatory markers, HPA-axis regulation, circadian rhythm and the antioxidant network are relevant nutritional targets in this state.

Focus Area 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
Mechanistic Hypotheses Under Investigation

Our research programme investigates for example whether catecholaminergic precursor availability, HPA-axis regulation, phospholipid synthesis, glucocorticoid-related stress signalling and prefrontal circuit function are relevant nutritional targets in this state.

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