Summary
Alzheimer’s disease is often discussed using two core pathologies:
- Amyloid (plaques)
- Tau (tangles)
They’re related — but not interchangeable.
This guide explains what each one is, what tests measure them, and why symptom onset doesn’t map perfectly to “how much plaque” alone.
What is amyloid?
Amyloid (especially Aβ42) can aggregate into plaques. In many models, amyloid changes appear early—often before symptoms.
Tests that can reflect amyloid include:
- amyloid PET imaging
- cerebrospinal fluid (CSF) Aβ42 (and ratios)
- plasma Aβ42/40 (in some settings)
What is tau?
Tau is a neuronal structural protein. In Alzheimer’s, tau becomes abnormally phosphorylated and can form tangles.
Tests that can reflect tau include:
- tau PET imaging
- CSF phosphorylated tau (p-tau)
- plasma p-tau biomarkers (including p-tau217)
Tau signals often track more closely with symptom severity than amyloid alone—especially once symptoms begin.
Why both matter
A simplified mental model:
- amyloid is an early “pathology marker”
- tau often tracks closer to neurodegeneration and symptoms
But symptoms depend on more than biomarkers:
- brain resilience and age
- vascular disease
- other co-pathologies
FAQ
If amyloid is positive, does that mean I have dementia?
No. Amyloid positivity can occur years before symptoms and must be interpreted in a clinical context.
Is tau a better predictor of symptoms than amyloid?
Tau biomarkers often correlate more closely with symptom severity than amyloid alone, especially around the time symptoms begin.
Are amyloid and tau the only causes of cognitive decline?
No. Age-related changes, vascular disease, medications, depression, sleep problems, and other neurodegenerative diseases can also contribute.
Related guides
Further reading
- NIH/NIA: https://www.nia.nih.gov/health/alzheimers
- Alzheimer’s Association: https://www.alz.org/alzheimers-dementia