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MediBalans›Cognitive Health & Alzheimer's
Prevention & Investigation · Stockholm
Cognitive Health · p-Tau217 · Neuroinflammation · Prevention

Alzheimer's begins
20 years before symptoms.

p-Tau217 is now the most accurate blood-based test for amyloid pathology — detectable 15–20 years before cognitive symptoms appear. MediBalans combines this with a complete biological mapping of the modifiable risk factors driving neurodegeneration: neuroinflammation, mitochondrial dysfunction, metabolomics and genetic profile.

>90%p-Tau217 sensitivity
20 yrsBefore clinical symptoms
14Modifiable risk factors

"There is no test for Alzheimer's until you have symptoms."
That is no longer true. p-Tau217 detects amyloid plaque formation in the brain from a blood sample — with precision previously requiring PET scanning or lumbar puncture. The window for meaningful intervention is the 15–20 years before symptoms appear.

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The biology of neurodegeneration

The modifiable drivers
behind Alzheimer's

Alzheimer's is not inevitable. It is the result of decades of biological processes — most of them measurable and addressable long before brain cells begin to die.

01

Neuroinflammation — the silent fire

ALCAT-identified food reactivities drive chronic cytokine production that crosses the blood-brain barrier. NF-κB-driven neuroinflammation activates microglia and drives amyloid-beta accumulation. This is the most underestimated and most modifiable risk factor for Alzheimer's.

02

Mitochondrial dysfunction — the brain's energy crisis

The brain consumes 20% of the body's energy. NutrEval organic acids reveal whether the Krebs cycle and electron transport chain are functioning in neuronal tissue. CoQ10 deficiency, carnitine deficiency and B-vitamin deficiencies are directly measurable and correctable.

03

Homocysteine and methylation capacity

Elevated homocysteine is one of the strongest blood-based risk markers for Alzheimer's and vascular dementia. Homocysteine is driven by MTHFR, MTR and MTRR variants reducing methylation cycle capacity. MethylDetox 38-gene panel maps this entire system.

04

Brain insulin resistance — type 3 diabetes

The brain's glucose utilisation declines 10–20 years before Alzheimer's diagnosis. NutrEval metabolomics reveals signs of cerebral energy metabolism disturbance. Brain insulin resistance is now recognised as a central mechanism — sometimes called type 3 diabetes.

05

APOE4 and lipid metabolism

The APOE4 allele is the strongest genetic risk factor for late-onset Alzheimer's — 3x increased risk with one copy, 12x with two copies. APOE4 affects amyloid clearance, lipid transport and neuronal repair. MethylDetox includes APOE genotyping as part of the neurological genetics panel.

06

p-Tau217 — the early warning system

Genova Diagnostics Alzheimer's Assessment #5400 measures p-Tau217 from a blood sample. Elevated levels indicate active amyloid plaque formation with >90% sensitivity. The test enables risk stratification and early intervention — not diagnosis after damage is done.

MediBalans protocol

Prevention and early intervention

MediBalans is the only clinic in Sweden combining the p-Tau217 risk biomarker with a complete biological mapping of the modifiable drivers. Knowing that p-Tau217 is elevated without knowing why — and without an intervention plan — is clinically insufficient.

As a clinical interpretation framework, GCR helps structure questions about possible risk factors such as inflammatory signals, metabolic patterns, genetic risk context and nutritional status. Test selection and prioritisation follow the clinical question; the framework cannot establish a root cause, optimal sequence or treatment effect on its own.

Who should test?

Family history of Alzheimer's or dementia. Cognitive fog or memory problems not explained by stress or poor sleep. APOE4 carriers wanting to understand their actual risk profile. Anyone over 45 wanting to map and optimise their neurological longevity.

Genova Diagnostics #5400

Alzheimer's Assessment — p-Tau217

The most precise blood-based test for amyloid pathology. p-Tau217 elevated 15–20 years before symptoms. Measurable from a simple blood draw. Pricing confirmed at consultation.

Genova Diagnostics #3000

NutrEval® Metabolomics

125+ metabolomic markers including organic acids revealing mitochondrial function, neurotransmitter metabolism and cellular energy production.

MediBalans

MethylDetox — 38 genes incl. APOE

APOE genotype, MTHFR, MTR, MTRR — complete neurological genetics profile. Homocysteine metabolism and genetic amyloid clearance capacity.

Cell Science Systems

ALCAT 250+ — Neuroinflammation

Food reactivities driving chronic neuroinflammation. The most modifiable risk factor — and the one standard care never measures.

Cell Science Systems

CMA — 55 intracellular markers

CoQ10, omega-3 index, magnesium, B12 and vitamin D — the neurological cofactors without which neuronal function and repair are compromised.

FAQ

Questions about cognitive investigation

p-Tau217 is a phosphorylated tau protein that reflects amyloid plaque formation in the brain. It rises in the blood 15–20 years before cognitive symptoms appear and has >90% sensitivity and specificity for Alzheimer's amyloid pathology — comparable to PET scanning and lumbar puncture, but from a blood sample. It is the most significant advance in Alzheimer's diagnostics in decades.
No. p-Tau217 is a risk biomarker — a measure of the probability of ongoing amyloid pathology. An elevated level indicates high risk and motivates deeper investigation and active intervention. It is not a diagnosis, and a normal level does not exclude all cognitive risk. The test is meaningful precisely because it provides a 15–20-year window for intervention.
Alzheimer's is not deterministic except in rare genetic forms (early-onset). The modifiable risk factors — neuroinflammation, mitochondrial dysfunction, homocysteine, insulin resistance and nutritional deficiencies — are well-studied and addressable. Intervention in the presymptomatic window (15–20 years before symptoms) is when biological effect is greatest.
APOE4 is the strongest genetic risk factor for late-onset Alzheimer's. One copy gives approximately 3x increased lifetime risk. Two copies approximately 12x. But APOE4 is not a death sentence — it is information. APOE4 carriers who optimise their modifiable risk factors consistently show better cognitive ageing than those who do not.
Preventive investigation is meaningful from age 40, especially with family history. With cognitive fog or memory problems, investigation is relevant at any age. p-Tau217 provides most value in the presymptomatic window — before clinical symptoms appear.
Related tests

Diagnostic protocols used in this investigation

Diagnostics
Alzheimer's Assessment — p-Tau217
Genova Diagnostics #5400. The most precise blood-based test for amyloid pathology. p-Tau217 elevated 15-20 years before symptoms.
Diagnostics
NutrEval® Metabolomics
125+ metabolomic markers. Mitochondrial function, neurotransmitter metabolism and homocysteine — the modifiable mechanisms behind cognitive decline.
Diagnostics
MethylDetox — 38 Genes
APOE genotype, MTHFR, MTR, MTRR. Complete neurological genetics profile — amyloid clearance capacity and homocysteine metabolism.
Diagnostics
ALCAT 250+ — Neuroinflammation
Food reactivities driving chronic neuroinflammation. The most modifiable risk factor for Alzheimer's — and the one standard care never measures.
Next step

Map your
cognitive risk profile

Book a consultation for complete cognitive risk assessment including p-Tau217, metabolomics, APOE genotype and modifiable risk factors.

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How BioAge and GCR are interpreted

BioAge compares RNA- and protein-related data in a model. It provides context and is not a diagnosis of a cognitive disorder. The GCR framework cannot establish a root cause on its own. Cognitive symptoms require an individual medical assessment.

Read the healthspan report and its limitations.

Explore the topic before your assessment