Key Benefits

• See how nutrients and blood fats affect brain aging and memory risk.
• Spot elevated homocysteine linked to cognitive decline and vascular dementia risk.
• Clarify reversible memory issues from B12 or folate deficiency and anemia.
• Guide targeted B12/folate therapy to lower homocysteine and support nerve function.
• Flag lipid patterns that raise stroke and small-vessel disease, worsening cognition.
• Track response as homocysteine falls with B vitamins and LDL improves with statins.
• Explain neuropathy, fatigue, or depression that may mimic Alzheimer’s symptoms.
• Interpret results with CBC, TSH, methylmalonic acid, and your symptoms.

What are Alzheimer’s Disease

Alzheimer’s disease biomarkers are objective signs of the disease’s biology in living people. They mirror the core brain changes that define the disease: buildup of amyloid plaques (amyloid-beta), spread of abnormal tau tangles (phosphorylated tau), and injury and loss of nerve cells (neurodegeneration). These proteins and related signals originate in the brain and can be detected in body fluids and on specialized brain scans, often years before memory problems appear. Biomarker testing turns a clinical suspicion into biology‑based evidence, helping confirm whether Alzheimer’s processes are present, distinguish it from other causes of cognitive decline, and gauge how far the disease has progressed. It also gives a way to monitor the brain’s response to therapy over time. Key readouts include amyloid measures that reflect plaque burden (Aβ), tau markers that track tangle formation and disease activity (p‑tau, total tau), and indicators of neuronal and synaptic damage (neurofilament light, neurogranin), alongside structural changes in the brain (atrophy). In short, biomarkers translate hidden brain pathology into measurable signals that guide diagnosis, prognosis, and care.

Why are Alzheimer’s Disease biomarkers important?

Alzheimer’s Disease biomarkers are measurable signs—from brain proteins to blood chemistry—that show how the brain is handling misfolded proteins, inflammation, energy use, and blood-vessel health. They matter because memory and thinking depend on intact neurons, steady nutrient supply, and clean vascular plumbing; when any of these systems strain, the brain’s resilience drops.

In blood, homocysteine typically sits around 5–15, and brain-friendly patterns tend toward the lower end. Vitamin B12 often spans 200–900, with cognition supported by the middle-to-upper range. Folate commonly runs 3–20, with the middle range adequate for one‑carbon metabolism. For lipids, LDL is often 70–160, HDL 40–60, and triglycerides 50–150; lower LDL and triglycerides with higher HDL generally favor cerebrovascular health.

When these markers fall below range, physiology shifts: low B12 or folate undermines myelin and DNA repair, often raising homocysteine, leading to numbness, imbalance, fatigue, mood changes, and memory lapses (megaloblastic anemia, neuropathy). Very low LDL or triglycerides can reflect poor intake or malabsorption and may compromise membrane and hormone synthesis, sometimes felt as weakness or weight loss. In pregnancy, low folate endangers fetal neural development; in children and teens, B12 deficiency can blunt growth and cognition.

At the high end, elevated homocysteine signals endothelial stress and small‑vessel injury linked to cognitive slowing and depression. High LDL or triglycerides accelerate atherosclerosis and white‑matter damage. Very high B12 can reflect liver or binding‑protein abnormalities; high folate with low B12 may mask anemia while neuropathy progresses. Men tend to have slightly higher homocysteine; after menopause, women’s LDL often rises.

Big picture: these biomarkers complement amyloid and tau by mapping the vascular‑metabolic terrain that shapes brain aging. Patterns favoring efficient methylation and healthy lipids align with better cerebrovascular function and, over time, a lower risk trajectory for cognitive decline.

What Insights Will I Get?

Alzheimer’s disease emerges from intersecting failures in energy production, vascular integrity, immune signaling, and synaptic maintenance. Biomarker testing maps these pathways before symptoms are obvious. At Superpower, we test Homocysteine, B12, Folate, and Lipids to profile one‑carbon metabolism and vascular–metabolic health linked to cognition.

Homocysteine is an intermediate of methylation; higher levels correlate with cognitive decline and vascular injury that amplify amyloid and tau stress. B12 (cobalamin) and Folate (vitamin B9) are cofactors that recycle homocysteine and support DNA synthesis, myelin, and neurotransmitter production; low levels are tied to cognitive impairment and neuropathy. Lipids (LDL, HDL, triglycerides) index lipid transport and vascular risk; dyslipidemia associates with small‑vessel disease, altered amyloid handling, and neuroinflammation.

For stability and healthy function: a balanced homocysteine suggests intact methylation capacity, endothelial health, and resilient neurons; elevations signal oxidative and vascular strain. Adequate B12 and folate indicate sufficient one‑carbon flux for genomic maintenance, myelination, and transmitter balance; insufficiency undermines synaptic stability and raises homocysteine. A favorable lipid profile supports membrane composition, lipid‑raft signaling, and cerebral perfusion; atherogenic patterns indicate cerebrovascular load that can accelerate neurodegeneration.

Notes: Age, kidney function, and thyroid status influence homocysteine. Pregnancy, anemia, and gastric disorders affect B12/folate; metformin, proton‑pump inhibitors, methotrexate, and anticonvulsants can shift levels. Fasting status, acute illness, and inflammation alter lipids; genetics (MTHFR, APOE) modify these pathways. Assay methods vary. These biomarkers inform risk biology but do not diagnose Alzheimer’s disease.