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.
GCR is used here as an interpretation framework for organising hypotheses around measured biomarkers such as homocysteine, omega-3 status, B6/B12 status and oxidative burden. The Alzheimer's Assessment measures a selected set of markers; it does not establish that one marker is the root cause, prove causality or determine treatment order or effect on its own.
