Visual field loss in senile dementia of the Alzheimer's type

Trick, Gary L.; Trick, Linda R.; Morris, Patricia; Wolf, Mitchell D.

doi:10.1212/wnl.45.1.68

Cited by 149 publications

(97 citation statements)

References 12 publications

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“…This is consistent with previous OCT findings 13, 15, 16, 17, 18, 20. The preferential loss of fibers in the superior quadrant is also compatible with the predominant inferior visual field defect documented in AD patients 56. It is intriguing that the superior sector contains the largest fibers of the optic nerve and previous postmortem studies documented a preferential loss of the larger axons, suggesting early involvement of the magnocellular RGCs in AD 11.…”

Section: Discussionsupporting

confidence: 91%

Melanopsin retinal ganglion cell loss in Alzheimer disease

Morgia

Ross‐Cisneros

Koronyo

et al. 2015

Annals of Neurology

321

397

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ObjectiveMelanopsin retinal ganglion cells (mRGCs) are photoreceptors driving circadian photoentrainment, and circadian dysfunction characterizes Alzheimer disease (AD). We investigated mRGCs in AD, hypothesizing that they contribute to circadian dysfunction.MethodsWe assessed retinal nerve fiber layer (RNFL) thickness by optical coherence tomography (OCT) in 21 mild‐moderate AD patients, and in a subgroup of 16 we evaluated rest–activity circadian rhythm by actigraphy. We studied postmortem mRGCs by immunohistochemistry in retinas, and axons in optic nerve cross‐sections of 14 neuropathologically confirmed AD patients. We coimmunostained for retinal amyloid β (Aβ) deposition and melanopsin to locate mRGCs. All AD cohorts were compared with age‐matched controls.ResultsWe demonstrated an age‐related optic neuropathy in AD by OCT, with a significant reduction of RNFL thickness (p = 0.038), more evident in the superior quadrant (p = 0.006). Axonal loss was confirmed in postmortem AD optic nerves. Abnormal circadian function characterized only a subgroup of AD patients. Sleep efficiency was significantly reduced in AD patients (p = 0.001). We also found a significant loss of mRGCs in postmortem AD retinal specimens (p = 0.003) across all ages and abnormal mRGC dendritic morphology and size (p = 0.003). In flat‐mounted AD retinas, Aβ accumulation was remarkably evident inside and around mRGCs.InterpretationWe show variable degrees of rest–activity circadian dysfunction in AD patients. We also demonstrate age‐related loss of optic nerve axons and specifically mRGC loss and pathology in postmortem AD retinal specimens, associated with Aβ deposition. These results all support the concept that mRGC degeneration is a contributor to circadian rhythm dysfunction in AD. ANN NEUROL 2016;79:90–109

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Section: Discussionsupporting

confidence: 91%

Melanopsin retinal ganglion cell loss in Alzheimer disease

Morgia

Ross‐Cisneros

Koronyo

et al. 2015

Annals of Neurology

321

397

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“…This region corresponds with the inferior visual field and these changes could explain the vision loss reported in this area in AD [48]. Other OCT studies have reported different patterns of RNFL loss (general, parapapillary and macular) [119,[135][136].…”

Section: (Figure 4)mentioning

confidence: 69%

“…Visual disturbance is often an early complaint of AD patients [46][47] and studies have reported reduced visual performance on tests of visual field [48][49], color vision [50][51][52], contrast sensitivity [53][54][55], backward masking [56][57], visual attention, motion perception, shape-from motion, visuo-spatial construction, visual memory [58][59][60], delayed saccadic initiation and movement and fixation problems [47,[61][62][63]. However, none of these deficiencies are specific to AD.…”

Section: Vision In Alzheimer's Diseasementioning

confidence: 99%

Ocular Biomarkers for Early Detection of Alzheimer's Disease

Frost

Martins

Kanagasingam

2010

JAD

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Alzheimer's disease (AD) is the most common form of dementia and is characterized clinically by a progressive decline in memory, learning and executive function and neuropathologically by the presence of cerebral amyloid deposits. Despite a century of research, there is still no cure or conclusive pre-mortem diagnosis for the disease. A number of symptom-modifying drugs for AD have been developed, but their efficacy is minimal and short-lived. AD cognitive symptoms arise only after significant, irreversible neural deterioration has occurred, hence there is an urgent need to detect AD early, before the onset of cognitive symptoms. An accurate, early diagnostic test for AD would enable current and future treatments to be more effective, as well as contribute to the development of new treatments.While most AD related pathology occurs in the brain, the disease has also been reported to affect the eye, which is more accessible for imaging than the brain. AD-related proteins exist in the normal human eye and may produce ocular pathology in AD. There is some homology between the retinal and cerebral vasculatures and the retina also contains nerve cells and fibers that form a sensory extension of the brain. The eye is the only place in the body where vasculature or neural tissue is available for non-invasive optical imaging. This article presents a review of current literature on ocular morphology in AD and discusses the potential for an ocular based screening test for AD.

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“…Alzheimer's disease may present with visual field loss 13 and more commonly field defects are recognised during the course of the disease. 14,15 However, presentation with reduced visual acuity is unusual.…”

Section: Discussionmentioning

confidence: 99%

Medically unexplained visual loss in adult patients

Griffiths

Eddyshaw

2004

Eye

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Purpose To evaluate the characteristics of patients with nonorganic or medically unexplained visual loss (MUVL) presenting to a neuro-ophthalmology clinic. Methods A retrospective review of the case notes of patients identified from our diagnostic register. All patients had been followed up for at least 18 months and investigations (including, in all cases, neuroimaging) had failed to reveal any underlying pathology. To be included, patients had to have at least one inconsistent feature on visual function testing. Results: We identified 58 patients with MUVL.

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Visual field loss in senile dementia of the Alzheimer's type

Cited by 149 publications

References 12 publications

Melanopsin retinal ganglion cell loss in Alzheimer disease

Melanopsin retinal ganglion cell loss in Alzheimer disease

Ocular Biomarkers for Early Detection of Alzheimer's Disease

Medically unexplained visual loss in adult patients

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