Vestibular Function and Beta-Amyloid Deposition in the Baltimore Longitudinal Study of Aging.

Dean F. Wong,Murat Bilgel,Rebecca J. Kamil,Susan M. Resnick,Yuri Agrawal

doi:10.3389/fnagi.2018.00408

Dean F. Wong, Murat Bilgel + Show 3 more

Open Access

https://doi.org/10.3389/fnagi.2018.00408

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Abstract

Beta-amyloid (Aβ) plaque deposition is a key feature of Alzheimer’s disease (AD), and occurs years before the onset of symptoms. Aβ plaque deposition has been shown to be present in ~30% of cognitively normal older adults using amyloid C-11 labeled Pittsburgh Compound B (11C-PiB) Positron Emission Tomography (PET) imaging. Prior studies have reported a link between reduced vestibular function and poorer cognition in healthy older adults. It is unknown whether vestibular impairment occurs in association with AD pathology among individuals in the preclinical phase of AD, which could contribute to the observed association between vestibular and cognitive function in healthy older adults. Using the Baltimore Longitudinal Study of Aging (BLSA), we analyzed the association between a comprehensive set of vestibular function measures and PiB status in 98 healthy participants with a mean age of 77.3 (±8.26). We did not observe a significant relationship between any vestibular function measure and PiB status in cognitively-intact older adults in the BLSA. This finding suggests that Aβ deposition does not explain the observed association between reduced vestibular function and poorer cognition in healthy older adults.

Highlights

Alzheimer’s disease (AD) is a neurodegenerative pathology that leads to memory loss and behavioral changes, and is fatal (Alzheimer’s Association, 2016)
Neither cervical vestibular-evoked myogenic potential (cVEMP) amplitude, ocular VEMP (oVEMP) amplitude, nor vestibular-ocular reflex (VOR) gain was significantly related to Pittsburgh Compound B (PiB) status
We did not observe a significant relationship between PiB status and vestibular function in 98 cognitively intact older adults in the Baltimore Longitudinal Study of Aging (BLSA)

Summary

Introduction

Alzheimer’s disease (AD) is a neurodegenerative pathology that leads to memory loss and behavioral changes, and is fatal (Alzheimer’s Association, 2016). One hypothesis for the pathogenesis of AD is that excessive extracellular Aβ accumulation causes synaptic dysfunction due to either a breakdown of Aβ clearance or Aβ overproduction (Hardy and Selkoe, 2002; Barage and Sonawane, 2015) This amyloid cascade hypothesis is controversial (Hardy and Selkoe, 2002; van Dyck, 2018). Increased Aβ deposition in cognitively normal adults has been associated with increased risk of decline on cognitive measures of visuospatial function, episodic and semantic memory, and mental status and increased risk of progression to AD (Mintun et al, 2006; Pike et al, 2007; Resnick et al, 2010; Vlassenko et al, 2011; Rowe et al, 2013; Baker et al, 2016)

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