Evidence map›Paper›PMID 41478826›Full record

ReviewThe journal of prevention of Alzheimer's disease2026

A review of evidence supporting amyloid beta reduction as a surrogate endpoint in Alzheimer's disease.

Tianle Chen, R Matthew Hutchison, Carrie Rubel, Jennifer Murphy, Jing Xie, John O'Gorman, Gersham Dent, Geert Molenberghs, Maria Pia Sormani, Suzanne Hendrix and 4 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The journal of prevention of Alzheimer's disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Longitudinal clinical outcomes after amyloid clearance in aducanumab phase 3 studies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Trial
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Tianle ChenBiogen, Inc, 225 Binney Street, Cambridge, MA, 02142, USA. Electronic address: tchen@kuraoncology.com.
R Matthew HutchisonBiogen, Inc, 225 Binney Street, Cambridge, MA, 02142, USA. Electronic address: matthew.hutchison@biogen.com.
Carrie RubelBiogen, Inc, 225 Binney Street, Cambridge, MA, 02142, USA. Electronic address: carrie.rubel@biogen.com.
Jennifer MurphyBiogen, Inc, 225 Binney Street, Cambridge, MA, 02142, USA. Electronic address: jennifer.murphy1@biogen.com.
Jing XieBiogen, Inc, 225 Binney Street, Cambridge, MA, 02142, USA. Electronic address: jing.xie@biogen.com.
John O'GormanBiogen, Inc, 225 Binney Street, Cambridge, MA, 02142, USA. Electronic address: john.ogorman@biogen.com.
Gersham DentBiogen, Inc, 225 Binney Street, Cambridge, MA, 02142, USA. Electronic address: gersham.dent@biogen.com.
Geert MolenberghsHasselt University, Martelarenlaan 42, 3500 Hasselt, Belgium; Katholieke Universiteit Leuven, Oude Markt 13, 3000 Leuven, Belgium. Electronic address: geert.molenberghs@uhasselt.be.
Maria Pia SormaniUniversity of Genoa, Via Balbi, 5, 16126 Genoa, Italy. Electronic address: mariapia.sormani@unige.it.
Suzanne HendrixPentara Corporation, 2261 E 3300 S, Millcreek, UT, 84109, USA. Electronic address: shendrix@pentara.com.
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Box 117, SE-221 00 Lund, Sweden. Electronic address: oskar.hansson@med.lu.se.
Paul AisenAlzheimer's Therapeutic Research Institute, Keck School of Medicine of University of Southern California, 9860 Mesa Rim Rd, San Diego, CA, 92121, USA. Electronic address: paisen@usc.edu.
Samantha Budd HaeberleinBiogen, Inc, 225 Binney Street, Cambridge, MA, 02142, USA. Electronic address: samanthaBH@pm.me.
Ying TianBiogen, Inc, 225 Binney Street, Cambridge, MA, 02142, USA. Electronic address: ytian01@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a heterogeneous neurodegenerative disease driven by pathological depositions of proteins that accumulate over decades. Compelling genetic and neurobiological evidence suggests that amyloid accumulation in the brain initiates and drives early-stage AD. Measurement of fibrillar amyloid has been pivotal to the development and approval of disease-slowing treatments. Various biomarkers of AD pathophysiology provide evidence of target engagement and downstream effects on disease progression, and their use as surrogate endpoints may help identify and expeditiously bring new treatments to patients. In clinical trials, a surrogate endpoint serves as a substitute for a direct measurement of a patient's clinical status, and its use can provide ethical, logistical, and economic advantages. Establishing biomarkers as surrogate endpoints involves evaluating scientific evidence through diverse statistical approaches to demonstrate their predictivity of clinical benefit. This article evaluated evidence supporting amyloid β plaque reduction as a surrogate endpoint in symptomatic AD by exploring regulatory considerations and guidelines for surrogate endpoints, examining the amyloid hypothesis and the current therapeutic landscape in AD, and presenting supporting evidence of surrogate endpoints from a recent clinical development program of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBiomarkersPlaque, AmyloidDisease ProgressionHumansAmyloid beta-PeptidesBiomarkersAlzheimer’s diseaseAmyloid βBiomarkerPositron emission tomographySurrogate endpoint

Identifiers

PMID41478826
PMCPMC12869041

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.