Key Benefits

'- Assess artery health and inflammation linked to vascular dementia from strokes and mini-strokes.

• Spot high ApoB and LDL that drive plaque reducing brain blood flow.
• Flag inherited Lp(a) elevations accelerating atherosclerosis and clot-related ischemic stroke risk lifelong.
• Clarify residual risk when LDL appears normal by counting particles with ApoB.
• Guide therapy intensity with ApoB and LDL targets, using hs-CRP as risk enhancer.
• Track response over time to reduce stroke recurrence and protect cognition long-term.
• Clarify lifelong risk with a once-in-a-lifetime Lp(a) measurement for prevention planning and monitoring.
• Best interpreted with blood pressure, A1c, smoking status, kidney function, and family history.

What are Dementia (Vascular)

Biomarker testing for vascular dementia reveals whether thinking and memory problems are being driven by diseased brain blood vessels and chronic shortfalls in blood flow. It captures the health of the vessel lining (endothelium), signals of vessel irritation (inflammation) and clotting activity (coagulation), and whether the brain’s filter has become leaky (blood–brain barrier). It also reads the downstream footprint of poor circulation: injury to nerve fibers (neuroaxonal damage; neurofilament light) and stress in support cells (astrocytes; GFAP). Imaging biomarkers add the map of accumulated harm, such as white matter scarring (white matter hyperintensities), tiny silent strokes (lacunes), and pinpoint bleeds (microbleeds) typical of small-vessel disease (cerebral small vessel disease). Together, these measures help detect a vascular contribution early, separate it from primarily degenerative causes like Alzheimer’s, gauge how active the process is now versus old scarring, and show which pathways are most at play—vessel injury, impaired perfusion, or nerve damage. That clarity enables targeted prevention and treatment aimed at protecting vessels, restoring blood flow, and slowing further brain injury.

Why are Dementia (Vascular) biomarkers important?

Vascular dementia biomarkers track the particles and inflammation that injure brain blood vessels. LDL, ApoB, and Lp(a) reflect the burden of atherogenic lipoproteins from the liver, while hs-CRP reflects whole‑body inflammatory tone from the immune system. Together they signal how likely arteries and small vessels are to narrow, clog, or inflame—processes that reduce cerebral blood flow, seed microinfarcts, and impair attention, planning, gait, and mood.

For context, labs often consider LDL desirable below about 100, ApoB below about 80–90, Lp(a) ideally below about 50 or 125 (assay-dependent), and hs-CRP best below 1, with persistent values above 3 concerning. For these markers, optimal generally sits toward the low end.

When these values are low, physiology is “quiet”: fewer ApoB-containing particles penetrate vessel walls, plaque growth slows, and inflammation is subdued. The brain’s white matter is better preserved, cognition feels clearer, and there are typically no symptoms. Very low Lp(a) is usually a benign genetic trait. In children and teens, low ApoB/Lp(a) suggests a lower lifetime vascular burden. During pregnancy, temporary shifts occur but symptom-free low levels remain reassuring.

When values trend high, lipoproteins enter and inflame vessel walls, plaques form and rupture risk rises, and hs-CRP flags active vascular inflammation. In the brain this shows up as small-vessel disease, white-matter changes, and stepwise declines after silent or overt strokes—slowed processing, executive dysfunction, gait instability, and mood changes. Men often accumulate risk earlier; women’s risk accelerates after menopause as LDL and Lp(a) rise; Lp(a) and hs-CRP can increase in pregnancy. In youth, elevated Lp(a) or ApoB is silent but raises lifetime stroke and vascular dementia risk.

Big picture: these biomarkers knit cardiovascular, hepatic, and immune biology into a single forecast of brain vascular health, complementing blood pressure, glucose, and kidney measures to anticipate long-term cognitive resilience or decline.

What Insights Will I Get?

Vascular dementia arises from impaired blood flow to brain tissue. Lipids and inflammation shape the health of cerebral vessels, the neurovascular unit, and the brain’s energy supply. At Superpower, we test LDL, ApoB, Lp(a), and hs-CRP to map atherogenic burden and inflammatory tone that influence cognitive resilience.

LDL is the cholesterol cargo; higher levels drive atherosclerotic plaque in brain arteries. ApoB counts atherogenic particles; higher ApoB signals greater endothelial injury potential. Lp(a) is a genetically determined LDL-like particle with apolipoprotein(a); it accelerates plaque and thrombosis. hs-CRP is a sensitive inflammation marker tied to vascular events and white-matter disease.

For stability, a lower LDL and ApoB profile means fewer particles entering vessel walls, supporting smoother cerebral perfusion and preserved cerebrovascular reserve. An Lp(a) that is not markedly elevated reduces prothrombotic, procalcific stress on brain vessels. A low hs-CRP reflects quieter innate immune activation, better endothelial function, and a more intact blood–brain barrier—conditions that lower microinfarcts and the downstream risk of vascular cognitive impairment.

Notes: Values are influenced by age, sex hormones (pregnancy, menopause), acute illness, and medications. Infections can transiently raise hs-CRP; acute inflammation may lower LDL. Lp(a) is largely genetic and stable; assay methods vary by isoform. Fasting has minimal impact on ApoB.