PH001 — Focus / Attention Stability
Capacity to sustain, shift, and regulate attention across changing cognitive demands.
How steadily a person can hold, shift, and return attention when tasks or distractions change.
Therapeutic areas: TA001 ★TA002TA004TA005TA006TA007
Provenance: Core Version 1 ADHD registry phenome (pre-v3). Benchmarked against RDoC Cognitive Systems (attention, cognitive control) and distinguished from Cognitive Clarity (PH011) as sustained/shifted attention versus processing clarity. (origin: BRAIN)
Related phenomes: PH002 — Motivation / Drive, PH011 — Cognitive Clarity
External framework cross-references
RDoC domains
- Cognitive Systems — attention
- Cognitive Systems — cognitive control
DSM / ICD context
- Attention-deficit/hyperactivity disorder
Foundational Evidence
Evidence Confidence: Low–Medium
Registry-level score for this phenome's foundational evidence stack — not Biology → Phenome Confidence on individual mechanism pages.
ADHD-focused construct and precursor-transport biology are well represented; human dietary attention-outcome evidence on the registry stack is indirect (omega-3 cognition trials) — not dietary ADHD treatment efficacy.
Registry-level foundational evidence for this phenome. Mechanism pages link to phenome IDs and carry relationship-specific evidence — not duplicated here.
Construct landmark papers
- Millichap & Yee (2012) — Reviews diet and nutritional factors in ADHD — foundational construct framing for attention phenotypes.
- Aquili (2020) — Reviews catecholaminergic neurotransmission and attentional function relevant to ADHD biology.
Biology → phenome landmark papers
- Fernstrom (2013) — Large neutral amino acid transport and precursor availability intersect monoaminergic attention pathways.
- Derbyshire & Maes (2023) — Links oxidative stress and neuroinflammation biology to ADHD symptom domains including attention.
Nutrition → biology landmark papers
- Wang et al. (2019) — Dietary patterns and amino-acid context modulate neurotransmitter precursor biology upstream of attention.
- Oulhaj et al. (2016) — Omega-3 supplementation associated with cognitive performance improvements in ageing — adjacent human nutrition→cognition support.
Connected mechanisms
- BRS-X(Hormones-PM1) — Oestrogen Signalling Stability (indirect · low-medium)
BRS1
- BRS1-FM1-PM1 — Amino-Acid Availability & Prioritisation (modulates · low-medium)
- BRS1-FM1-PM2 — LAT1 Competitive Transport Modulation (modulates · low-medium)
- BRS1-FM1-PM3 — Noradrenergic Signalling (modulates · high)
- BRS1-FM2-PM5 — Acetylcholine Synthesis Support (modulates · low-medium)
- BRS1-FM3-PM6 — Neuronal Membrane DHA Incorporation (modulates · low-medium)
- BRS1-FM4-PM7 — GABA–Glutamate Neurotransmission Balance (modulates · high)
- BRS1-FM4-PM9 — Glutamate Clearance & Recycling (modulates · low-medium)
BRS2
- BRS2-FM1-PM1 — Folate/B12-Dependent Homocysteine Remethylation (modulates · low-medium)
- BRS2-FM1-PM2 — Betaine/BHMT Remethylation (modulates · low-medium)
- BRS2-FM1-PM4 — Methionine Cycle Flux (modulates · low-medium)
- BRS2-FM3-PM7 — Phosphatidylcholine Formation (modulates · low-medium)
BRS3
- BRS3-FM1-PM1 — NF-kB Signalling Regulation (modulates · low-medium)
- BRS3-FM1-PM2 — Gut-Derived Inflammatory Signalling (modulates · low-medium)
- BRS3-FM2-PM3 — Nrf2-ARE Antioxidant Activation (modulates · low-medium)
- BRS3-FM2-PM4 — ROS Generation vs Clearance Balance (modulates · low-medium)
- BRS3-FM2-PM5 — Lipid Peroxidation Control (modulates · low-medium)
- BRS3-FM3-PM7 — Cytokine Network Modulation (modulates · low-medium)
- BRS3-FM3-PM8 — Eicosanoid / SPM Balance (modulates · low)