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. 2022 Dec 17;12(12):1729.
doi: 10.3390/brainsci12121729.

Aβ42 as a Biomarker of Alzheimer's Disease: Is Saliva a Viable Alternative to Cerebrospinal Fluid?

Silvia Boschi  1 , Fausto Roveta  1 , Alberto Grassini  1 , Andrea Marcinnò  1 , Aurora Cermelli  1 , Fabio Ferrandes  1 , Innocenzo Rainero  1 , Elisa Rubino  1
Affiliations

Aβ42 as a Biomarker of Alzheimer's Disease: Is Saliva a Viable Alternative to Cerebrospinal Fluid?

Silvia Boschi et al. Brain Sci. .

Abstract

The identification of reliable biomarkers in biological fluids is paramount to optimizing the diagnosis of Alzheimer’s disease (AD). Measurement of Aβ42, t-tau, and p-tau in cerebrospinal fluid (CSF) is the most accepted method to support the diagnosis of AD. However, lumbar puncture represents an invasive investigation, whereas saliva is one of the most accessible body fluids. The aim of our study was to investigate salivary concentrations in AD and evaluate the correlation between salivary and CSF Aβ42 concentrations in AD patients, patients with non-AD dementias, and controls. We recruited 100 subjects: 18 AD patients, 64 patients with non-AD dementias, and 18 controls. The mean saliva Aβ42 concentrations in AD patients were higher than in controls (p < 0.001), and to patients with non-AD dementias (p = 0.001). A significant negative correlation between salivary and CSF Aβ42 concentrations was found in the overall group (r = −0.562, p < 0.001) and in non-AD patients (r = −0.443, p < 0.001). Salivary Aβ42 concentrations positively correlated with CSF t-tau (r = 0.321, p = 0.001) and p-tau (r = 0.297, p = 0.001). Our study showed that in AD patients’ saliva, Aβ42 concentrations are specifically increased, and we found an interesting negative correlation between CSF and salivary Aβ42 concentrations that warrants further investigation.

Keywords: Alzheimer’s disease; CSF; beta amyloid 42; biomarkers; saliva.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The hypothetical interaction linking the pathological processes of Alzheimer’s disease at the brain level and pathological amyloid-β fragments at the salivary level. This figure was made with Biorender.com.
Figure 2
Figure 2
Comparison of salivary Aβ42 concentrations between AD, non-AD, and controls. Data were shown as mean ± SD.
Figure 3
Figure 3
ROC curve of salivary Aβ42 concentrations for the diagnosis of AD.
Figure 4
Figure 4
Correlation between salivary Aβ42 concentrations and CSF Aβ42 concentrations (A) in the overall population (r = −0.562, p < 0.001); (B) in the non-AD group (r = −0.443, p < 0.001); and (C) in the AD group (r = −0.205, p = 0.415).
Figure 4
Figure 4
Correlation between salivary Aβ42 concentrations and CSF Aβ42 concentrations (A) in the overall population (r = −0.562, p < 0.001); (B) in the non-AD group (r = −0.443, p < 0.001); and (C) in the AD group (r = −0.205, p = 0.415).
See this image and copyright information in PMC

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