Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/209718
Title: Light-Induced Pupillary Responses in Alzheimer's Disease
Authors: Chougule, Pratik S
Najjar Raymond 
Finkelstein, Maxwell T
Kandiah, Nagaendran 
Milea, D. 
Keywords: Science & Technology
Life Sciences & Biomedicine
Clinical Neurology
Neurosciences
Neurosciences & Neurology
Alzheimer's disease
dementia
pupillary light response
chromatic pupillometry
melanopsin expressing intrinsically photosensitive retinal ganglion cells
Parkinson's disease
post -Ilumination pupil response
cholinergic deficit
RETINAL GANGLION-CELLS
NORADRENERGIC LOCUS-COERULEUS
EDINGER-WESTPHAL NUCLEUS
FUNCTIONAL NEUROANATOMY
CHOLINERGIC HYPOTHESIS
CEREBROSPINAL-FLUID
PARKINSONS-DISEASE
FLICKER PHOTOMETRY
COGNITIVE DECLINE
ALPHA-SYNUCLEIN
Issue Date: 12-Apr-2019
Publisher: FRONTIERS MEDIA SA
Citation: Chougule, Pratik S, Najjar Raymond, Finkelstein, Maxwell T, Kandiah, Nagaendran, Milea, D. (2019-04-12). Light-Induced Pupillary Responses in Alzheimer's Disease. FRONTIERS IN NEUROLOGY 10 (APR). ScholarBank@NUS Repository.
Abstract: The impact of Alzheimer's disease (AD) on the pupillary light response (PLR) is controversial, being dependent on the stage of the disease and on the experimental pupillometric protocols. The main hypothesis driving pupillometry research in AD is based on the concept that the AD-related neurodegeneration affects both the parasympathetic and the sympathetic arms of the PLR (cholinergic and noradrenergic theory), combined with additional alterations of the afferent limb, involving the melanopsin expressing retinal ganglion cells (mRGCs), subserving the PLR. Only a few studies have evaluated the value of pupillometry as a potential biomarker in AD, providing various results compatible with parasympathetic dysfunction, displaying increased latency of pupillary constriction to light, decreased constriction amplitude, faster redilation after light offset, decreased maximum velocity of constriction (MCV) and maximum constriction acceleration (MCA) compared to controls. Decreased MCV and MCA appeared to be the most accurate of all PLR parameters allowing differentiation between AD and healthy controls while increased post-illumination pupillary response was the most consistent feature, however, these results could not be replicated by more recent studies, focusing on early and pre-clinical stages of the disease. Whether static or dynamic pupillometry yields useful biomarkers for AD screening or diagnosis remains unclear. In this review, we synopsize the current knowledge on pupillometric features in AD and other neurodegenerative diseases, and discuss potential roles of pupillometry in AD detection, diagnosis and monitoring, alone or in combination with additional biomarkers.
Source Title: FRONTIERS IN NEUROLOGY
URI: https://scholarbank.nus.edu.sg/handle/10635/209718
ISSN: 16642295
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