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Updated: Jan 7, 2026

Dried Blood Spot Collection of Health Biomarkers to Maximize Participation in Population Studies

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Published on: January 28, 2014

Biomarkers.

Marie Emilie Tuil¹, Bshaier Allehyany², Rifa Sanjida Punnota²

¹Imperial College London, London, United Kingdom.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association

|December 25, 2025

Summary

This summary is machine-generated.

Microglial responses in Alzheimer's disease (AD) vary by stage. Early stages show neurotoxic amyloid-beta dependent microglial activity, while later stages shift towards neuroprotection, then back to neurotoxicity as pathology progresses.

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Area of Science:

Neuroscience
Immunology
Neuropathology

Background:

Microglial activation is central to Alzheimer's disease (AD) pathology, but its precise role is debated.
Evidence suggests both neurotoxic and neuroprotective functions of microglia in AD.
TREM2 mutations, a risk factor, impair microglial response, while certain microglial phenotypes appear protective.

Purpose of the Study:

To investigate the association between AD biomarkers and cognitive function.
To understand how microglial responses impact AD pathology across different disease stages.

Main Methods:

Analysis of 323 participants from the ADNI database.
Stratification into Aβ+AD, Aβ+MCI, and Aβ-MCI groups.
Utilized CSF biomarkers (sTREM2, GAP-43, Aβ_1-42, T-tau, p-tau₁₈₁), MRI, PET scans, and cognitive scores (ADAS-Cog-13).

Main Results:

TREM2 showed significant associations with tau and Aβ_1-42 in MCI stages, but not in AD.
A negative association between amyloid and cognitive scores was observed in Aβ+MCI.
GAP43 was associated with Aβ_1-42 in MCI and AD stages.

Conclusions:

Microglial responses in AD are distinct and stage-dependent.
An amyloid-beta dependent neurotoxic microglial response occurs in early MCI.
A neuroprotective microglial phenotype emerges in response to amyloid in MCI, with a return to neurotoxicity in later AD stages.