Process atlas

A visual way into biology: choose a topic, look at the process, then open the explanation when you need more detail.

Normal physiology, research associations and individual clinical conclusions are different kinds of information. Each diagram names its scope and links its sources. The images are educational schematics rather than diagnostic tests or personal treatment instructions.

Overview and genetic evidence

Whole system overviewAn organising frameworkGenes regulation and developmentEvidence interpretationLarge scale brain networksEvidence interpretationCognitive functions and observable outcomesEvidence interpretationDevelopment synapse formation and maintenanceEvidence interpretationContextual genetic overlayEvidence interpretationCommon locus to effector gene evidenceEvidence interpretation framework

Supply, synthesis and cofactors

Amino acid supply and brain entryScoped educational mechanismCatecholamine synthesis and cell type branchesScoped educational mechanismBH4 synthesis and cofactor recyclingScoped educational mechanismVitamin and mineral supportScoped educational mechanismSerotonin supply and transmissionScoped educational mechanismOne carbon metabolism and methyl donorsScoped educational mechanismTH reaction and regulationScoped educational mechanismDBH and PNMT compartment detailScoped educational mechanismBH4 hydroxylase recycling and salvageScoped educational mechanism

Synapses and receptor signalling

Vesicle loading and storageEstablished transport mechanismRelease and vesicle recyclingScoped educational mechanismSynaptic clearance and intracellular metabolismScoped educational mechanismReceptors and intracellular responseScoped educational mechanismGlutamate transmissionScoped educational mechanismGABA transmission and inhibitionScoped educational mechanismAcetylcholine and attention modulationScoped educational mechanismAstrocytes and transmitter recyclingScoped educational mechanismDAT uptake and ion gradientsScoped educational mechanismPFC receptor signalling in a defined contextScoped educational mechanismGlutamate glutamine cellular shuttleScoped educational mechanism

Energy and cellular support

Energy supply and neuronal demandScoped educational mechanismRedox balance and glutathioneScoped educational mechanismMitochondrial quality control: one mitophagy routeScoped educational mechanismImmune signalling and neural contextEvidence interpretationBlood flow oxygen and glucose deliveryScoped educational mechanismMitochondrial membrane and respiratory chainEstablished cellular mechanism

Context and arousal

Dopamine and noradrenaline projection systemsScoped educational mechanismSleep circadian timing and arousalScoped educational mechanismAdrenal hormones: two tissue compartmentsScoped educational mechanismNutrition: supply, transport and evidence limitsScoped educational mechanismHistamine and orexin arousal modulesScoped educational mechanism

Medicine handling and targets

Medication absorption metabolism and eliminationScoped educational mechanismMedication target overlaysScoped educational mechanismAmphetamine dexamfetamine at the dopamine terminalScoped educational mechanism

Four starting points

Whole system overview

An organising framework

Whole system overview. Read from genes and regulation through development, precursor supply, cellular energy, synaptic communication and brain circuits to cognitive performance.
How do biology and context connect to cognitive function? This is an organising model, not one ADHD formula or a diagnostic graph.MJB ADHD Process Atlas · Reviewed 2026-10-13

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Read from genes and regulation through development, precursor supply, cellular energy, synaptic communication and brain circuits to cognitive performance. Sleep, stress and environment are additional inputs. The connecting arrows organise relationships for learning; they do not demonstrate one causal chain, one defect shared by everybody with ADHD or a diagnostic test.

Vesicle loading and storage

Established transport mechanism

Vesicle loading and storage. ATP hydrolysis powers the vesicular proton pump, V-ATPase, which acidifies the vesicle.
ATP powers the vesicle's proton pump. VMAT2 uses the resulting proton gradient to load monoamines for storage and later release; it is not directly powered by ATP. This normal mechanism does not establish an individual transport defect.MJB ADHD Process Atlas · Reviewed 2026-10-13

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ATP hydrolysis powers the vesicular proton pump, V-ATPase, which acidifies the vesicle. VMAT2 exchanges vesicular protons for cytosolic monoamines such as dopamine. It therefore uses an existing proton gradient rather than directly hydrolysing ATP itself. Stored transmitter can subsequently be released by exocytosis. This explains a normal mechanism, not evidence of a VMAT2 defect in a particular reader.

Mitochondrial membrane and respiratory chain

Established cellular mechanism

Mitochondrial membrane and respiratory chain. NADH supplies electrons through complex I, while succinate oxidation supplies electrons through complex II.
Electrons pass along the respiratory chain while complexes I, III and IV pump protons. Proton return through ATP synthase supports ATP formation. This illustrates general cell physiology; it does not establish an energy defect in a reader.MJB ADHD Process Atlas · Reviewed 2026-10-13

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NADH supplies electrons through complex I, while succinate oxidation supplies electrons through complex II. Ubiquinone transfers electrons to complex III, cytochrome c carries them to complex IV, and oxygen is the final acceptor. Complexes I, III and IV pump protons from the matrix towards the intermembrane space. Complex II is membrane-bound but does not pump protons; its label is placed on the matrix side in this simplified drawing. Proton return through ATP synthase supports ATP formation from ADP and phosphate. The diagram does not establish mitochondrial dysfunction in ADHD.

Common locus to effector gene evidence

Evidence interpretation framework

Common locus to effector gene evidence. Begin with an associated locus, then evaluate fine-mapping, candidate variants, regulatory or coding consequences, potential effector genes and tissue-specific functions.
A genetic association identifies a region of interest. Connecting it to a candidate variant, gene and tissue-specific process requires several kinds of evidence. Each step has uncertainty; proximity alone does not establish causality.MJB ADHD Process Atlas · Reviewed 2026-10-13

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Begin with an associated locus, then evaluate fine-mapping, candidate variants, regulatory or coding consequences, potential effector genes and tissue-specific functions. Each step needs its own evidence. Linkage disequilibrium can leave several correlated candidates, and regulation may act over a distance. Proximity can be a clue but does not establish the causal gene by itself. These are complementary evidence types, not a mandatory sequence or a validated causal conclusion about one person.

Three different evidence questions

Three different evidence questions. A mechanism, an association and an individual conclusion are different kinds of evidence. A connection between these questions needs evidence; it is not automatic.
Use the question to recognise the scope of a claim. A normal pathway does not prove a defect; an association does not prove an individual cause.

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A mechanism, an association and an individual conclusion are different kinds of evidence.

  • Mechanism: How can a biological process work? Enzymes, transporters, cells and model experiments.
  • Association: What varies together in a study? A statistical result needs its sample, effect and uncertainty.
  • Individual conclusion: What does this mean for this person? Clinical and genetic interpretation needs additional evidence.

A connection between these questions needs evidence; it is not automatic.