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= Disease Entity = Alzheimer disease (AD) is a primary progressive neurodegenerative disease affecting approximately 4.7% of individuals age 60 years. AD is typically characterized by deterioration of memory and other neurocognitive functions that ultimately interferes with daily life and is can be fatal. AD is the most common form of dementia, accounting for over 50% of cases. In the United States, 5.5 million people are affected and and up to 35 million worldwide have the disease<ref>Querfurth, H. W. & LaFerla, F. M. Alzheimer’s Disease. ''N. Engl. J. Med.'' '''362''', 329–344 (2010).</ref><ref name=":0">Prince, M. ''et al.'' The global prevalence of dementia: A systematic review and metaanalysis. ''Alzheimers Dement. J.Alzheimers Assoc.'' '''9''', 63–75.e2 (2013).</ref>. There is currently no cure for AD but there are treatments with variable and modest efficacy <ref name=":1">Weiner, M. W. ''et al.'' The Alzheimer’s Disease Neuroimaging Initiative: A review of papers published since its inception. ''Alzheimers Dement. J. Alzheimers Assoc.'' '''8''', S1-68 (2012).</ref>. == Pathophysiology == AD is believed to arise from the accumulation of misfolded proteins that induces oxidative and secondary inflammatory damage on the aging brain leading to cognitive decline. Specific pathological features of AD include β-amyloid (Aβ) peptide plaques and tau protein neurofibrillary tangles (NFT). According to the predominant ‘amyloid hypothesis,’ Aβ precipitates secondary to an imbalance between production and clearance such that there is an accumulation and aggregation of Aβ2. NFT are formed from the intracellular aggregation of abnormal tau proteins. The number of NFT correlates with disease severity. Secondary inflammation and oxidative stress may interfere with synaptic and neuronal activity, leading to neuronal loss and brain atrophy<ref name=":0" /><ref name=":1" /><ref name=":2">Heneka, M. T. ''et al.'' Neuroinflammation in Alzheimer’s disease. ''Lancet Neurol.'' '''14''', 388–405 (2015).</ref>. = Diagnosis = As visualization of Aβ and NFT via brain imaging is of limited specificity and resolution, AD diagnosis is primarily clinical with reliance on a range of testing modalities ranging from cognitive assessments and physical exam to brain imaging (MRI, CT, PET). Definitive diagnosis is only through postmortem histological exam with visualization of NFT and Aβ<ref name=":1" /><ref>Perl, D. P. Neuropathology of Alzheimer’s Disease. ''Mt. Sinai J. Med. N. Y.'' '''77''', 32–42 (2010).</ref>. == Physical examination == The ophthalmic findings reported in AD patients are summarized below (from Colligris et al. and Javaid et al).<ref>Javaid, F. Z., Brenton, J., Guo, L. & Cordeiro, M. F. Visual and Ocular Manifestations of Alzheimer’s Disease and Their Use as Biomarkers for Diagnosis and Progression. ''Front. Neurol.'' '''7''', (2016).</ref><ref>Colligris, P., Perez de Lara, M. J., Colligris, B. & Pintor, J. Ocular Manifestations of Alzheimer’s and Other Neurodegenerative Diseases: The Prospect of the Eye as a Tool for the Early Diagnosis of Alzheimer’s Disease. ''J. Ophthalmol.'' '''2018''', (2018).</ref>. {| class="wikitable" !Ocular Structures !'''Pathological Changes in AD''' |- |'''Retina''' |<nowiki>- Deposition of proteins tau, Aβ and pTAu</nowiki><ref>Schön, C. ''et al.''Long-term in vivo imaging of fibrillar tau in the retina of P301S transgenic mice. ''PloS One'' '''7''', e53547 (2012).</ref><ref name=":3">Alexandrov, P. N., Pogue, A., Bhattacharjee, S. & Lukiw, W. J. Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer’s disease. ''Neuroreport'' '''22''', 623–627 (2011).</ref><ref>Koronyo, Y. ''et al.'' Retinal amyloid pathology and proof-of-concept imaging trial in Alzheimer’s disease. ''JCI Insight'' '''2''', (2017).</ref><ref name=":4">Koronyo, Y., Salumbides, B. C., Black, K. L. & Koronyo-Hamaoui, M. Alzheimer’s disease in the retina: imaging retinal aβ plaques for early diagnosis and therapy assessment. ''Neurodegener. Dis.'' '''10''', 285–293 (2012).</ref>- Impaired metabolism of amyloid β precursor protein (APP)<ref>Gao, L. ''et al.''Neuroprotective effect of memantine on the retinal ganglion cells of APPswe/PS</ref><ref name=":5">Rusu, P. ''et al.'' Axonal accumulation of synaptic markers in APP transgenic Drosophila depends on the NPTY motif and is paralleled by defects in synaptic plasticity. ''Eur. J.'' Neurosci.'' '''25''', 1079–1086 (2007).''</ref><ref>Dutescu, R. M. ''et al.'' Amyloid precursor protein processing and retinal pathology in mouse models of Alzheimer’s disease. ''Graefes'' Arch. Clin. Exp. Ophthalmol. Albrecht Von Graefes Arch. Klin. Exp. Ophthalmol.''<nowiki/>'' '''247''', 1213–1221 (2009).</ref> <nowiki> </nowiki>- Reduction in retinal ganglion cells<ref name=":6">Sadun, A. A. & Bassi, C. J. Optic nerve damage in Alzheimer’s disease. ''Ophthalmology'' '''97''', 9–17 (1990).</ref><ref>Blanks, J. C., Hinton, D. R., Sadun, A. A. & Miller, C. A. Retinal ganglion cell degeneration in Alzheimer’s disease. ''Brain'' Res.'' '''501''', 364–372 (1989).'' </ref><ref>Hinton, D. R., Sadun, A. A., Blanks, J. C. & Miller, C. A. Optic-nerve degeneration in Alzheimer’s disease. ''N. Engl. J. Med.'' '''315''', 485–487 (1986).</ref> - Reduction of retinal thickness<ref name=":6" /><ref>Trebbastoni, A. ''et'' al.'' Retinal nerve fibre layer thickness changes in Alzheimer’s disease: R''</ref><ref>Parisi, V. ''et al.'' Morphological and functional retinal impairment in Alzheimer’s disease patients. ''Clin. Neurophysiol. Off. J. Int. Fed. Clin. Neurophysiol.'' '''112''', 1860–1867 (2001).</ref> - Reduction in the retinal nerve fiber layer thickness (RNFL)<ref>Hedges, T. R. ''et'' al.'' Retinal nerve fiber layer abnormalities in Alzheimer’s disease. ''Acta Ophthalmol. Scand.'' '''74''', 271–275 (1996).''</ref><ref>Coppola, G. ''et al.'' Optical Coherence Tomography in Alzheimer’s Disease: A Meta-Analysis. ''PloS One'' '''10''', e0134750 (2015).</ref><ref>Berisha, F., Feke, G. T., Trempe, C. L., McMeel, J. W. & Schepens, C. L. Retinal abnormalities in early Alzheimer’s disease. ''Invest. Ophthalmol. Vis. Sci.'' '''48''', 2285–2289 (2007).</ref> - Retrograde degeneration secondary to loss of cortical neurons<ref>Burke, W. J. ''et'' al.'' Evidence for retrograde degeneration of epinephrine neurons in'' Alzheimer’s disease. ''Ann. Neurol.'' '''24''', 532–536 (1988).</ref><ref>Mutlu, U. ''et al.'' Association of Retinal Neurodegeneration on Optical Coherence Tomography With Dementia: A Population-Based Study. ''JAMA Neurol.'' '''75''', 1256–1263 (2018).</ref> - Inflammation<ref name=":2" /><ref>Swanson, A., Wolf, T., Sitzmann, A. & Willette, A. A. Neuroinflammation in Alzheimer’s disease: Pleiotropic roles for cytokines and neuronal pentraxins. ''Behav.'' Brain Res.'' '''347''', 49–56 (2018).''</ref> |- |'''Retinal and choroidal vasculature''' |<nowiki>- Retinal and choroidal vascular β-amyloid deposits in transgenic mouse model of AD lead to retinal degeneration</nowiki><ref>Ning, A., Cui, J., To, E., Ashe, K. H. & Matsubara, J. Amyloid-beta deposits lead to retinal degeneration in a mouse model of Alzheimer disease. ''Invest. Ophthalmol. Vis.'' Sci.'' '''49''', 5136–5143 (2008).''</ref>- Impaired vascularization<ref>Paris, D. ''et al.''Impaired angiogenesis in a transgenic mouse model of cerebral amyloidosis. ''Neurosci.'' Lett.'' '''366''', 80–85 (2004).''</ref> |- |'''Retinal vascular blood flow''' |<nowiki>- Blood flow disturbances can lead to neurodegeneration</nowiki><ref>Feke, G. T., Hyman, B. T., Stern, R. A. & Pasquale, L. R. Retinal blood flow in mild cognitive impairment and Alzheimer’s disease. ''Alzheimers Dement. Amst. Neth.'' '''1''', 144–151 (2015).</ref> |- |'''Optic nerve''' |<nowiki>- Axonal degeneration in the axonal segments</nowiki><ref name=":5" /><ref name=":6" />- Loss of optic nerve thickness<ref>Kesler, A., Vakhapova, V., Korczyn, A. D., Naftaliev, E. & Neudorfer, M. Retinal thickness in patients with mild cognitive impairment and Alzheimer’s disease. ''Clin. Neurol. Neurosurg.'' '''113''', 523–526 (2011).</ref><ref>Tsai, C. S. ''et al.'' Optic nerve head and nerve fiber layer in Alzheimer’s disease. ''Arch.'' Ophthalmol. Chic. Ill 1960'' '''109''', 199–204 (1991).''</ref> - Papillary paleness due to axonal loss and perfusion alterations<ref>Bambo, M. P. ''et'' al.'' Analysis of optic disk color changes in Alzheimer’s disease: a'' potential new biomarker. ''Clin. Neurol. Neurosurg.'' '''132''', 68–73 (2015).</ref> |- |'''Lens''' |<nowiki>- Correlation between AD and supranuclear cataract</nowiki><ref name=":7">Tian, T., Zhang, B., Jia, Y. & Li, Z. Promise and challenge: the lens model as a biomarker for early diagnosis of Alzheimer’s disease. ''Dis. Markers'' '''2014''', 826503 (2014).</ref><ref name=":8">Liu, S. S. & Zhu, S. Q. [Correlation between Alzheimer disease and cataract]. ''Zhonghua Yan Ke Za Zhi Chin. J. Ophthalmol.'' '''53''', 314–316 (2017).</ref>- Presence of abnormal protein deposits<ref name=":8" /><ref name=":9">Kerbage, C., Sadowsky, C. H., Jennings, D., Cagle, G. D. & Hartung, P. D. Alzheimer’s disease diagnosis by detecting exogenous fluorescent signal of ligand bound to Beta amyloid in the lens of human eye: an exploratory study. ''Front. Neurol.'' '''4''', 62 (2013).</ref> |- |'''Tears''' |<nowiki>- Changes in the chemical barrier composition of tears</nowiki><ref name=":10">Kalló, G. ''et al.'' Changes in the Chemical Barrier Composition of Tears in Alzheimer’s Disease Reveal Potential Tear Diagnostic Biomarkers. ''PloS One'' '''11''', e0158000 (2016).</ref> |- |'''Cornea''' |<nowiki>- Reduced corneal sensitivity</nowiki><ref>Örnek, N., Dağ, E. & Örnek, K. Corneal sensitivity and tear function in neurodegenerative diseases. ''Curr. Eye Res.'' '''40''', 423–428 (2015).</ref> |- |'''Pupil''' |<nowiki>- Pupillary response, possible biomarker</nowiki><ref name=":11">Granholm, E. L. ''et al.'' Pupillary Responses as a Biomarker of Early Risk for Alzheimer’s Disease. ''J. Alzheimers Dis. JAD'' '''56''', 1419–1428 (2017).</ref> |- |'''Choroid''' |<nowiki>- Attenuation of choroidal thickness</nowiki><ref>Trebbastoni, A. ''et'' al.'' Attenuation of Choroidal Thickness in Patients With Alzheimer Disease:'' Evidence From an Italian Prospective Study. ''Alzheimer Dis. Assoc. Disord.'' '''31''', 128–134 (2017).</ref> |} {| class="wikitable" !Visual Function !'''Pathological Changes in AD''' |- |'''Visual fields''' |<nowiki>- Inferior hemifield loss</nowiki><ref>Trick, G. L., Trick, L. R., Morris, P. & Wolf, M. Visual field loss in senile dementia of the Alzheimer’s type. ''Neurology'' '''45''', 68–74 (1995).</ref><ref>Gilmore, G. C. & Levy, J. A. Spatial contrast sensitivity in Alzheimer’s disease: a comparison o</ref> |- |'''Visual acuity''' |<nowiki>- Decreased visual acuity in low luminance</nowiki><ref>Cormack, F. K., Tovee, M. & Ballard, C. Contrast sensitivity and visual acuity in patients with Alzheimer’s disease. ''Int. J. Geriatr. Psychiatry'' '''15''', 614–620 (2000).</ref><ref>Lakshminarayanan, V., Lagrave, J., Kean, M. L., Dick, M. & Shankle, R. Vision in dementia: contrast effects. ''Neurol.'' Res.'' '''18''', 9–15 (1996).''</ref><ref name=":12">Polo, V. ''et al.'' Visual dysfunction and its correlation with retinal changes in patients with Alzheimer’s disease. ''Eye Lond. Engl.'' '''31''', 1034–1041 (2017).</ref> |- |'''Sensory perception''' |<nowiki>- Clinically important symptoms of visuospatial disorientation</nowiki><ref name=":12" /><ref>Thiyagesh, S. N. ''et'' al.'' The neural basis of visuospatial perception in Alzheimer’s disease and'' healthy elderly comparison subjects: an fMRI study. ''Psychiatry Res.'' '''172''', 109–116 (2009).</ref> |- |'''Visual processing''' |<nowiki>- Deficits of visual motion perception</nowiki><ref>Mapstone, M., Dickerson, K. & Duffy, C. J. Distinct mechanisms of impairment in cognitive ageing and Alzheimer’s disease. ''Brain J. Neurol.'' '''131''', 1618–1629 (2008).</ref> |- |'''Contrast sensitivity''' |<nowiki>- Contrast sensitivity disturbances and motion perception</nowiki><ref>Rizzo, M. & Nawrot, M. Perception of movement and shape in Alzheimer’s disease. ''Brain J.'' Neurol.'' '''121 ( Pt 12)''', 2259–2270 (1998).''</ref><ref>Gilmore, G. C., Wenk, H. E., Naylor, L. A. & Koss, E. Motion perception and Alzheimer’s disease. ''J.'' Gerontol.'' '''49''', P52-57 (1994).''</ref> |- |'''Color vision''' |<nowiki>- Color discrimination error inversely proportional with mini-mental state examination (MMSE) score</nowiki><ref>Salamone, G. ''et al.'' Color discrimination performance in patients with Alzheimer’s disease. ''Dement. Geriatr. Cogn.'' Disord.'' '''27''', 501–507 (2009).''</ref> |- |'''Stereopsis''' |<nowiki>- Reduced stereoscopic depth perception</nowiki><ref>Mittenberg, W., Malloy, M., Petrick, J. & Knee, K. Impaired depth perception discriminates Alzheimer’s dementia from aging and major depression. ''Arch. Clin.'' Neuropsychol.'' '''9''', 71–79 (1994).''</ref> |- |'''Circadian rhythm''' |<nowiki>- Alterations in the circadian rhythm and β-amyloid deposits inside and surrounding degenerating mRGCs</nowiki><ref>Musiek, E. S., Xiong, D. D. & Holtzman, D. M. Sleep, circadian rhythms, and the pathogenesis of Alzheimer disease. ''Exp.'' Mol. Med.'' '''47''', e148 (2015).''</ref><ref>La Morgia, C., Ross-Cisneros, F. N., Sadun, A. A. & Carelli, V. Retinal Ganglion Cells and Circadian Rhythms in Alzheimer’s Disease, Parkinson’s Disease, and Beyond. ''Front.'' Neurol.'' '''8''', 162 (2017).''</ref><ref>Feng, R., Li, L., Yu, H., Liu, M. & Zhao, W. Melanopsin retinal ganglion cell loss and circadian dysfunction in Alzheimer’s disease (Review). ''Mol. Med. Rep.'' '''13''', 3397–3400 </ref> |} Of note, the visual variant of AD (VVAD), also known as posterior cortical atrophy (PCA), is characterized by prominent visual symptoms due to localized atrophy of the parieto-occipital lobe. VVAD is For more information, please see corresponding EyeWiki [https://eyewiki.org/Visual_variant_of_Alzheimer%E2%80%99s_disease article]. Patients with PCA typically present with difficulty reading or problems with visuospatial and visual processing. A homonymous hemianopsia or cortical visual loss with a negative structural imaging study (e.g., MRI) or neuroimaging showing only posterior cortical atrophy may suggest the diagnosis of AD. == Diagnostic procedures == '''Imaging''' Previously, retinal OCT imaging in AD patients noted NFL layer atrophy and ganglion cell death<ref>Jindahra, P., Hedges, T. R., Mendoza-Santiesteban, C. E. & Plant, G. T. Optical coherence tomography of the retina: applications in neurology. ''Curr. Opin. Neurol.'' '''23''', 16–23 (2010).</ref><ref>La Morgia, C. ''et al.'' Melanopsin retinal ganglion cell loss in Alzheimer disease. ''Ann. Neurol.'' '''79''', 90–109 (2016).</ref> . However, these findings were not specific to AD and were also reported in other neurodegenerative disorders (e.g., Parkinson disease). Reduced RNFL thickness on OCT has been associated with memory deficits<ref>Méndez-Gómez, J. L. ''et al.'' Peripapillary Retinal Nerve Fiber Layer Thickness and the Evolution of Cognitive Performance in an Elderly Population. ''Front. Neurol.'' '''8''', 93 (2017).</ref>. Recent studies have reported detection of hallmark Aβ plaques in the retina in AD patients via scanning laser ophthalmoscope using the natural fluorochrome curcumin that binds to the plaques<ref name=":3" /><ref>Jiang, J., Wang, H., Li, W., Cao, X. & Li, C. Amyloid Plaques in Retina for Diagnosis in Alzheimer’s Patients: a Meta-Analysis. ''Front. Aging Neurosci.'' '''8''', (2016).</ref><ref>Koronyo-Hamaoui, M. ''et al.'' Identification of Amyloid Plaques in Retinas from Alzheimer’s Patients and Noninvasive In Vivo Optical Imaging of Retinal Plaques in a Mouse Model. ''NeuroImage'' '''54S1''', S204–S217 (2011).</ref> . Fluorescence is quantified via an automated calculation of the retinal amyloid index (RAI). Compared to healthy controls, AD patients had a 2.1-fold increase in fluorescent intensity over baseline. Furthermore, the fluorescence pattern is consistent with histological data showing Aβ deposits clustered in the peripheral superior quadrant, often along blood vessels<ref name=":3" />. Retinal vascular parameters (RVPs) may also serve as a tool for early AD diagnosis <ref>Frost, S. ''et al.'' Retinal vascular biomarkers for early detection and monitoring of Alzheimer’s disease. ''Transl. Psychiatry'' '''3''', e233 (2013).</ref>. The decreased retinal microvascular network density noted in AD patients suggests retinal vessel reaction to flicker stimulation, delayed in AD patients, could be another potential non-invasive biomarker<ref>Kotliar, K. ''et al.'' Altered neurovascular coupling as measured by optical imaging: a biomarker for Alzheimer’s disease. ''Sci. Rep.'' '''7''', 12906 (2017).</ref><ref>Jiang, H. ''et al.'' Altered Macular Microvasculature in Mild Cognitive Impairment and Alzheimer Disease. ''J. Neuro-Ophthalmol. Off. J. North Am. Neuro-Ophthalmol. Soc.'' '''38''', 292–298 (2018).</ref>. '''Optical coherence tomography angiography (OCTA)''' <nowiki> </nowiki>OCTA has also been used on AD patients to detect decreased retinal vasculature density as well as reduced retinal and choroidal flow rates<ref>Baumann, B. ''et al.'' Visualization of neuritic plaques in Alzheimer’s disease by polarization-sensitive optical coherence microscopy. ''Sci. Rep.'' '''7''', 43477 (2017).</ref><ref>Bulut, M. ''et al.'' Evaluation of optical coherence tomography angiographic findings in Alzheimer’s type dementia. ''Br. J. Ophthalmol.'' '''102''', 233–237 (2018).</ref> . The metabolic hyperspectral retinal camera is another device currently being studied for its biomarker potential via measurement of regional retinal vessel oxygen saturation. This device utilizes 225 contiguous spectral bands collected at high speeds to localize biomolecules and structures based on their respective spectral signatures<ref>Shahidi, A. M., Patel, S. R., Flanagan, J. G. & Hudson, C. Regional variation in human retinal vessel oxygen saturation. ''Exp. Eye Res.'' '''113''', 143–147 (2013).</ref><ref>Mordant, D. J. ''et al.'' Oxygen saturation measurements of the retinal vasculature in treated asymmetrical primary open-angle glaucoma using hyperspectral imaging. ''Eye Lond. Engl.'' '''28''', 1190–1200 (2014).</ref>. Another study evaluating the association between type 2 diabetes and AD employs microperimetry to measure retinal neurodegeneration. Microperimetry assesses retinal sensitivity by measuring the minimum light intensity which the patients can perceive by stimulating specific areas of retina with spots of light<ref>Ciudin, A. ''et al.'' Retinal Microperimetry: A New Tool for Identifying Patients With Type 2 Diabetes at Risk for Developing Alzheimer Disease. ''Diabetes'' '''66''', 3098–3104 (2017).</ref>. <nowiki> </nowiki>Another target for AD detection is the pathologic hyperphosphorylated Tau protein (NFT), which has been detected in postmortem human retinas and AD human models in the absence of tau aggregation, suggesting a pre-symptomatic disease stage<ref name=":4" /><ref>Spires-Jones, T. L., Stoothoff, W. H., de Calignon, A., Jones, P. B. & Hyman, B. T. Tau pathophysiology in neurodegeneration: a tangled issue. ''Trends Neurosci.'' '''32''', 150–159 (2009).</ref><ref>Chiasseu, M. ''et al.'' Tau accumulation in the retina promotes early neuronal dysfunction and precedes brain pathology in a mouse model of Alzheimer’s disease. ''Mol. Neurodegener.'' '''12''', 58 (2017).</ref>. '''Lens''' Studies have detected β-amyloid in the lens of human AD patients as well as correlation between cortical cataracts and AD degeneration<ref name=":7" /><ref name=":9" />. A clinical trial is currently evaluating the use of aftobetin hydrochloride, a topical amyloid-binding compound to detect β-amyloid in patients with mild cognitive impairment and mild AD (ClinicalTrials.gov Identifier: NCT02928211). T'''ear Fluid''' AD patients have been reported to have increased tear flow rate and protein levels. The presence of lipocalin-1, dermicidin, lysozyme C and lactritin had an 81% sensitivity and 77% specificity for AD35<ref name=":10" />. '''Pupillary Light Response and Eye Movement''' Pupillary light reflex amplitude has been noted to be decreased in AD<ref name=":11" /><ref>Tales, A. ''et al.'' The pupillary light reflex in aging and Alzheimer’s disease. ''Aging Milan Italy'' '''13''', 473–478 (2001).</ref>. There is also an ongoing study to track eye movements as an AD diagnostic tool, with previous studies showing delayed saccadic eye movement and smooth ocular pursuit<ref>Sadun, A. A., Borchert, M., DeVita, E., Hinton, D. R. & Bassi, C. J. Assessment of visual impairment in patients with Alzheimer’s disease. ''Am. J. Ophthalmol.'' '''104''', 113–120 (1987).</ref><ref>Fletcher, W. A. & Sharpe, J. A. Smooth pursuit dysfunction in Alzheimer’s disease. ''Neurology'' '''38''', 272–277 (1988).</ref> (ClinicalTrials.gov Identifier: NCT01434940). == Implications == While still in development, this wide range of AD detection modalities are promising as a specific, early and noninvasive method of objective AD diagnosis, with potential for prognostication as well. = References = <references />
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