Abstract
To assess and compare the involvement of choroidal thickness (CT) in patients with mild cognitive impairment (MCI) and dementia due to Alzheimer's disease (AD) defined by amyloid PET and healthy controls (HC). Sixty-three eyes from 34 AD patients [12 eyes (19.0%) with dementia and 51 eyes (80.9%) with MCI], positive to 11C-labelled Pittsburgh Compound-B with positron emission tomography (11C-PiB PET/CT), and the same number of sex- and age-paired HC were recruited. All participants underwent enhanced depth imaging optical coherence tomography (EDI-OCT) assessing CT at 14 measurements from 2 B-scans. Paired Student t-test was used to compare CT measurements between MCI, dementia and sex- and age-paired HC. A univariate generalized estimating equations model (GEE) test was performed to compare MCI and dementia individually with all HC included. Compared with HC, eyes from patients with positive 11C-PiB PET/CT showed a significant CT thinning in 5 selected locations (in foveal thickness in vertical scan, in temporal scan at 1500μm, in superior scan at 500μm and in inferior scan at 1000μm and 1500μm, p = 0.020-0.045) whilst few significant CT reduction data was reported in MCI or dementia individually versus HC. However, the GEE test identified significant CT thinning in AD compared with all HC included (p = 0.015-0.046). To our knowledge, the present study is the first measuring CT in eyes from MCI and dementia eyes positive to 11C-PiB PET/CT reporting a significant trend towards CT thinning in MCI patients which became more pronounced in dementia stage. We support further investigation involving larger and prospective OCT studies in AD population characterized with available biomarkers to describe whether choroidal vascular damage occurs specifically in prodromal stages of AD.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disorder and is the most common cause of dementia and one of the leading sources of morbidity and mortality in the aging population [1]
The present study is the first measuring choroidal thickness (CT) in eyes from mild cognitive impairment (MCI) and dementia eyes positive to 11C-labeled Pittsburgh Compound-B (11C-PiB) positron emission tomography/computed tomography (PET/CT) reporting a significant trend towards CT thinning in MCI patients which became more pronounced in dementia stage
We support further investigation involving larger and prospective Optical coherence tomography (OCT) studies in AD population characterized with available biomarkers to describe whether choroidal vascular damage occurs in prodromal stages of AD
Summary
Alzheimer’s disease (AD) is a neurodegenerative disorder and is the most common cause of dementia and one of the leading sources of morbidity and mortality in the aging population [1]. The hallmark neuropathologic changes of AD are extracellular beta amyloid beta plaques and neurofibrillary tangles (NFT) comprised of intracellular hyperphosphorylated tau protein (p-tau). These neuropathological changes are believed to start 15–20 years before the onset of clinical symptoms of dementia [3]. Aβ protein brain deposition is detected by decreased 42–amino acid form of Aβ (Aβ-42) levels in cerebrospinal fluid (CSF) and positron emission tomography/computed tomography (PET/CT) imaging using 11C-labeled Pittsburgh Compound-B (11C-PiB) ligand [3, 7], which is the most studied and validated PET marker of Aβ. Restrictions still exist in clinical practice (such as standardization problems and invasiveness in the case of CSF markers, and high costs and limited availability in the case of amyloid PET) and they are not yet recommended for routine diagnostic purposes [10, 13]
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