The Study
Aβ deposition is associated with increases in soluble and phosphorylated tau that precede a positive Tau PET in Alzheimer’s disease
This study watched people over time and saw that when the brain starts making too much amyloid (a sticky protein), it also starts changing another protein called tau in the fluid around the brain — but the bad tau clumps don’t show up on scans until years later. It’s like seeing smoke before the fire starts, but we can’t say the smoke caused the fire — just that they often happen together.
Analysis score
Maximum 72 for a cohort study.
Where the score came from
Before the brain forms sticky tau tangles, a soluble form of tau in spinal fluid starts rising — but only if amyloid plaques are already present.
Where does this study sit?
Reviews of RCTs (Meta-analyses)
Max 100Randomized Trials
Max 90Reviews of Cohort Studies
Max 85Cohort Studies
Max 72Reviews of Case-Control Studies
Max 63Case-Control Studies
Max 58Cross-Sectional & Case Series
Max 50Expert Opinion
Max 554 / 100
Quality score
Groups of people are followed over time to see who develops an outcome. Strong for identifying risk factors and associations, but cannot prove causation as firmly as RCTs.
Key takeaways
Summary
Based on the study abstract and findings.
- 1This means doctors could detect Alzheimer’s risk years earlier by testing spinal fluid for P-tau217 — before memory problems or brain scans show damage.
- 2P-tau217 rises 12 years before tau tangles show up on PET scans; it increases even before amyloid PET is officially positive; 70% of people with amyloid plaques have high P-tau217 before tau PET turns positive.
Score breakdown, methodology, conflicts of interest, evidence analysis & raw study data
Publication
Journal
Science Advances
Year
2020
Authors
N. Mattsson‐Carlgren, E. Andersson, S. Janelidze, R. Ossenkoppele, P. Insel, O. Strandberg, H. Zetterberg, H. Rosen, G. Rabinovici, Xiyun Chai, K. Blennow, Jeffrey L. Dage, E. Stomrud, Ruben Smith, S. Palmqvist, O. Hansson
Related Content
Claims (6)
Phosphorylated tau protein can be detected in the brain using neuroimaging techniques 12 years before a person shows any signs of Alzheimer's disease.
Levels of phosphorylated tau proteins in cerebrospinal fluid account for 68–82% of the connection between amyloid-beta buildup and the formation of neurofibrillary tangles in the brain.
In people with early Alzheimer's-related brain changes but no cognitive symptoms, phosphorylated tau proteins in spinal fluid rise before tau clumps become visible on brain scans, with phosphorylated tau-217 increasing first and most strongly.
In people with early amyloid buildup in the brain, a specific form of tau protein called P-tau217 increases in cerebrospinal fluid before amyloid PET scans show abnormal levels.
People with a genetic mutation that causes tau protein to clump in the brain but who do not have amyloid-beta plaques have normal levels of phosphorylated tau in their spinal fluid, showing that this specific tau modification requires amyloid-beta to occur.
In genetically modified mice that develop amyloid plaques but not tau tangles, levels of soluble tau in the cerebrospinal fluid rise as amyloid-beta accumulates, showing that amyloid pathology can trigger soluble tau release without the presence of tau aggregates.
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.