BACKGROUND: Neurodegenerative diseases share retinal abnormalities. Chromatic pupillometry allows in vivo assessment of photoreceptor functional integrity, including melanopsin-expressing retinal ganglion cells. This exploratory meta-analysis assesses retinal photoreceptor functionality in Alzheimer\'s vs. Parkinson\'s disease and conducts an in-depth review of applied pupillometric protocols.
METHODS: Literature reviews on PubMed and Scopus from 1991 to August 2023 identified chromatic pupillometry studies on Alzheimer\'s disease (AD; n = 42 patients from 2 studies) and Parkinson\'s disease (PD; n = 66 from 3 studies). Additionally, a pre-AD study (n = 10) and an isolated REM Sleep Behavior Disorder study (iRBD; n = 10) were found, but their results were not included in the meta-analysis statistics.
RESULTS: Melanopsin-mediated post-illumination pupil response to blue light was not significantly impaired in Alzheimer\'s (weighted mean difference = -1.54, 95% CI: 4.57 to 1.49, z = -1.00, p = 0.319) but was in Parkinson\'s (weighted mean difference = -9.14, 95% CI: 14.19 to -4.08, z = -3.54, p < 0.001). Other pupil light reflex metrics showed no significant differences compared to controls. Studies adhered to international standards of pupillometry with moderate to low bias. All studies used full-field stimulation. Alzheimer\'s studies used direct while Parkinson\'s studies used consensual measurement. Notably, studies did not control for circadian timing and Parkinson\'s patients were on dopaminergic treatment.
CONCLUSIONS: Results affirm chromatic pupillometry as a useful method to assess melanopsin-related retinal cell dysfunction in Parkinson\'s but not in Alzheimer\'s disease. While adhering to international standards, future studies may analyze the effects of local field stimulation, dopaminergic treatment, and longitudinal design to elucidate melanopsin dysfunction in Parkinson\'s disease.

To provide an updated overview of Photophobia with a particular focus on photophobia related to migraine.
Melanopsin-containing photoreceptors called intrinsically photosensitive retinal ganglion cells (ipRGCs) have been identified in the retina and explain the rational for photophobia in individuals who are blind. Photophobia, a sensory disturbance provoked by light, is a common neurological and ophthalmological symptom. Migraine, a common neurological condition, is pathognomonic of photophobia; however, other primary headache conditions, traumatic brain injury, and impairment of the optic pathway can cause photophobia. In addition, anterior and posterior segment ocular pathology, medications, and psychiatric conditions can result in photophobia. At least 2 (possibly three) distinct neural pathways are involved in photophobia. Some of the basic science regarding these pathways is discussed in this review including the role of calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating polypeptide. Management of photophobia includes treatment of the underlying etiology and conservative strategies such as wearing sunglasses.

Alzheimer\'s disease affects 27 million individuals and is the most common cause of dementia worldwide. The pathology of Alzheimer\'s disease is primarily due to the β‑amyloid deposits and neurofibrillary tangles. These deposits exist largely in the cerebral blood vessels, but have also been shown to exist in retinal vessels. A new class of cells that were recently identified, known as melanopsin‑expressing retinal ganglion cells (mRGCs), are involved in the non‑image forming functions of the eye. These functions include circadian activities such as temperature rhythms, melatonin release and rest‑activity cycles. Circadian dysfunction has been investigated in many cases of Alzheimer\'s disease. In this review, we outline the current accepted Alzheimer\'s disease pathology, the role of mRCGs in optic neuropathies and the role of mRCGs, leading to circadian dysfunction, in Alzheimer\'s disease.

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