Alzheimer's disease has a genetic component — APOE4 is the most studied variant — but genetics accounts for a minority of cases. The majority of Alzheimer's risk is metabolic, vascular and nutritional in origin: correctable biochemical imbalances that accumulate over decades before clinical symptoms appear.
Homocysteine is among the most robustly documented. A meta-analysis of 77 studies found that elevated homocysteine is independently associated with a 2–3× increased risk of Alzheimer's disease. It damages cerebral vessels, promotes tau hyperphosphorylation, impairs myelin synthesis, and is directly associated with accelerated brain volume loss on MRI. It is almost always correctable — but correction requires knowing which B-vitamin pathway is driving it.
DHA is equally important. The brain is approximately 60% lipid by dry weight, and DHA constitutes 30–40% of grey matter fatty acids. Low Omega-3 Index is associated with reduced hippocampal volume, accelerated cognitive aging and increased amyloid-beta accumulation.
The GCR framework applies directly to cognitive aging: every identified modifiable biomarker — homocysteine, omega-3 deficiency, B6/B12 insufficiency, oxidative burden — represents a constraint on cognitive resilience. Addressing the highest-burden constraints systematically is more effective than supplementing a single nutrient in isolation. The Alzheimer's Assessment identifies which constraints are active. The protocol addresses them in priority order.