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Purpose <p>The aim of this study was to compare regional brain tau extent across the disease spectrum in early- and late-onset Alzheimer’s disease using the second-generation tau PET tracer [<sup>18</sup>F]RO948, and to investigate the relationship between PET-derived patterns, plasma p-tau217, brain atrophy, and cognition.</p> Methods <p>We examined 57 participants: 39 patients from the Cognitive Assessment Unit at Karolinska University Hospital (Stockholm/Sweden)—diagnosed as MCI Aβ– (<i>n</i> = 10), MCI Aβ + (<i>n</i> = 16; 8 EO and 6 LO), and AD (<i>n</i> = 13; 5 EOAD and 8 LOAD)—and 18 cognitively normal controls. All participants underwent [<sup>18</sup>F]RO948 tau-PET, structural MRI, cognitive testing, and plasma p-tau217 analysis.</p> Results <p>Both EO and LO MCI (Aß +) showed higher [<sup>18</sup>F]RO948 binding in amygdala, entorhinal cortex, hippocampus (<i>p</i> &lt; 0.001) and extending to inferior temporal regions (<i>p</i> &lt; 0.01) compared to controls, with some MCI-EO cases already showing advanced neocortical tau burden. At the AD stage, EOAD patients showed greater neocortical tau extent in temporo-parietal and frontal cortices than LOAD. P‑tau217 positively correlated with [<sup>18</sup>F]RO948 in amygdala, entorhinal cortex, hippocampus (rho = 0.81) followed by temporal (rho = 0.71), and parietal cortices (rho = 0.56, all <i>p</i> &lt; 0.001). The Tau‑PET/p-tau217 association was different between EOAD and LOAD with greater differences in parietal cortices. Tau‑PET also showed stronger region‑specific associations with cognitive impairment than p‑tau217, especially in EOAD.</p> Conclusions <p>[<sup>18</sup>F]RO948-PET captured interindividual heterogeneity in tau accumulation that was not reflected by plasma p-tau217. This dissociation was particularly evident in neocortical regions, where LOAD showed elevated plasma p-tau217 levels despite low tau PET binding. These findings highlight the value of tau-PET as a sensitive biomarker for detecting early disease heterogeneity, assessing disease severity, and improving patient stratification for disease-modifying treatments.</p>

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[18F]RO948 Tau PET in early and late onset Alzheimer’s disease: associations with plasma p-tau 217, atrophy and cognition

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月26日

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  • Mariola Zapater-Fajari,
  • Marco Bucci,
  • Konstantinos Chiotis,
  • Ove Almkvist,
  • Anders Wall,
  • Jonas Eriksson,
  • Gunnar Antoni,
  • Ilaria Pola,
  • Kübra Tan,
  • Wiebke Traichel,
  • Andrea L. Benedet,
  • Nicholas J. Ashton,
  • Henrik Zetterberg,
  • Nenad Bogdanovic,
  • Agneta Nordberg

摘要

Purpose

The aim of this study was to compare regional brain tau extent across the disease spectrum in early- and late-onset Alzheimer’s disease using the second-generation tau PET tracer [18F]RO948, and to investigate the relationship between PET-derived patterns, plasma p-tau217, brain atrophy, and cognition.

Methods

We examined 57 participants: 39 patients from the Cognitive Assessment Unit at Karolinska University Hospital (Stockholm/Sweden)—diagnosed as MCI Aβ– (n = 10), MCI Aβ + (n = 16; 8 EO and 6 LO), and AD (n = 13; 5 EOAD and 8 LOAD)—and 18 cognitively normal controls. All participants underwent [18F]RO948 tau-PET, structural MRI, cognitive testing, and plasma p-tau217 analysis.

Results

Both EO and LO MCI (Aß +) showed higher [18F]RO948 binding in amygdala, entorhinal cortex, hippocampus (p < 0.001) and extending to inferior temporal regions (p < 0.01) compared to controls, with some MCI-EO cases already showing advanced neocortical tau burden. At the AD stage, EOAD patients showed greater neocortical tau extent in temporo-parietal and frontal cortices than LOAD. P‑tau217 positively correlated with [18F]RO948 in amygdala, entorhinal cortex, hippocampus (rho = 0.81) followed by temporal (rho = 0.71), and parietal cortices (rho = 0.56, all p < 0.001). The Tau‑PET/p-tau217 association was different between EOAD and LOAD with greater differences in parietal cortices. Tau‑PET also showed stronger region‑specific associations with cognitive impairment than p‑tau217, especially in EOAD.

Conclusions

[18F]RO948-PET captured interindividual heterogeneity in tau accumulation that was not reflected by plasma p-tau217. This dissociation was particularly evident in neocortical regions, where LOAD showed elevated plasma p-tau217 levels despite low tau PET binding. These findings highlight the value of tau-PET as a sensitive biomarker for detecting early disease heterogeneity, assessing disease severity, and improving patient stratification for disease-modifying treatments.