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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.

Tatsuya Manabe¹, Takuto Iida¹, Takashi Saito¹

¹Nagoya City University, Nagoya, Aichi, Japan.

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

|December 25, 2025

Summary

Chronic kidney disease (CKD) in aged mice elevates brain tau phosphorylation, suggesting a kidney-brain axis. This research explores how CKD impacts tau pathology and neuroinflammation in aging populations.

Area of Science:

Neuroscience
Nephrology
Biochemistry

Background:

Alzheimer's disease (AD) is characterized by beta-amyloid (Aβ) plaques.
Phosphorylated tau protein (p-tau) is a biomarker for Aβ burden, with blood levels of p-tau181 and p-tau217 indicating preclinical AD.
Chronic kidney disease (CKD) can elevate p-tau independently of Aβ pathology.

Purpose of the Study:

Investigate the link between CKD and elevated circulating p-tau.
Determine if CKD-induced brain p-tau elevation contributes to increased blood p-tau.
Utilize a mouse model to understand the kidney-brain axis in CKD.

Main Methods:

Induced CKD in mice using an adenine-rich diet.
Assessed renal function via histology and biochemical markers.

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Evaluated brain tau phosphorylation (p-tau181, p-tau217, p-tau396) using western blot.

Quantified microglial morphology to assess neuroinflammation.

Main Results:

Adenine induced renal fibrosis and elevated plasma uremic toxins, with age-dependent severity.
Aged CKD mice exhibited heightened levels of p-tau181, p-tau217, and p-tau396 in the brain.
CKD led to reduced microglial ramification in aged mice, indicating neuroinflammation.

Conclusions:

Adenine successfully modeled CKD pathology within six weeks.
Aged mice showed more severe renal dysfunction and delayed recovery.
Altered brain p-tau and neuroinflammation in aged CKD mice highlight a novel kidney-brain axis relevant to elderly patients.