Neurodegeneration of the retina in mouse models of Alzheimer’s disease: what can we learn from the retina?

Chiu, Kin; Chan, Tat Ming Danny; Wu, Anhua; Leung, Irene; So, Kwok-Fai; Chang, Raymond Chuen‐Chung

doi:10.1007/s11357-011-9260-2

Cited by 85 publications

(70 citation statements)

References 112 publications

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“…The retina is a central nervous system tissue, originating as an outgrowth of the developing brain. It contains highdensity neuronal cells and fibers that form its sensory extension [51,[53][54][55][56] . Some homology between retinal and brain vasculatures has also been described; retinal vasculature is argued to be a direct extension of its cerebral counterpart [51,53] .…”

Section: The Retina: a Window To View Ad?mentioning

confidence: 99%

Alzheimer’s Disease in the Retina: Imaging Retinal Aβ Plaques for Early Diagnosis and Therapy Assessment

et al. 2012

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Background: Definite Alzheimer’s disease (AD) diagnosis at early stages is vital for targeting intervention, yet currently unavailable. Noninvasive detection of the pathological hallmark, amyloid-β protein (Aβ) plaques, is limited in the brain. However, the existence of Aβ plaques in the retina, possibly at presymptomatic stages, may improve early detection of AD. Objective: To summarize clinical and preclinical evidence showing that the retina, an accessible part of the central nervous system, displays abnormalities in AD, especially Aβ plaque pathology. The ability to monitor in vivo retinal plaque dynamics in response to immunotherapy is also assessed. Methods: Literature analysis of retinal AD pathology and imaging is provided. In our studies, systemic curcumin is administered to enable monitoring of retinal Aβ plaques in live APP_SWE/PS1_Δ_E9 transgenic mice by optical imaging. Results: Visual and retinal abnormalities, including early manifestation of retinal Aβ plaque pathology, have been documented in AD patients and animal models. In mouse models, retinal Aβ plaques accumulate with age and decrease in response to immunotherapy, consistent with brain pathology. Here, we demonstrate that retinal plaques can be individually monitored in real time following glatiramer acetate immunization. Conclusion: Translation of noninvasive retinal-plaque imaging to humans could eventually facilitate early and accurate AD diagnosis and therapy assessment.

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Section: The Retina: a Window To View Ad?mentioning

confidence: 99%

Alzheimer’s Disease in the Retina: Imaging Retinal Aβ Plaques for Early Diagnosis and Therapy Assessment

et al. 2012

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“…26 The retina is composed of 10 layers, one of them being the nerve fibre layer. The latter layer is part of the Figure 1.…”

Section: Discussionmentioning

confidence: 99%

Macular Thickness in Subjective Memory Complaints and Mild Cognitive Impairment: A Non-Invasive Biomarker

Castejón

Dudekova

Gallego

et al. 2016

Neuro-Ophthalmology

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Alzheimer's disease (AD) is the main cause of dementia worldwide, which implies an important socioeconomic problem in developed countries. Efforts to find biomarkers to diagnose AD have been intensified, especially, to detect cognitive impairment in its early stages, also known as mild cognitive impairment (MCI). Besides, there are individuals referring memory loss that is unnoticeable in the family environment and presenting normal neuropsychological tests. The former patients are included in a clinical picture that has been recently called subjective memory complaints (SMC). To achieve an early diagnosis, optical coherence tomography (OCT) has been used to measure macular thickness in patients diagnosed with MCI (supported by neuropsychological tests) and SMC (not based on neuropsychological battery). Statistically significant differences have been found in the macular thickness of the control group (274.96 ± 17.61 µm) and for both MCI (259.48 ± 22.39 µm) and SMC (261.45 ± 24.26 µm) patients. In the near future, OCT could become a reliable biomarker and a useful tool for AD screening as well as for the monitoring of the cognitive impairment associated with AD. ARTICLE HISTORY

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“…Glaucoma is defined as a group of disorders characterized by optic neuropathy with clinically visible alterations at the ONH encompassing thinning of the neuroretinal rim and excavation of the optic disc and representing progressive loss of RGCs and their axons [58].…”

Section: Glaucomamentioning

confidence: 99%

Contribution of microglia‐mediated neuroinflammation to retinal degenerative diseases

Boia

Madeira

Aires

et al. 2017

Acta Ophthalmologica

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Retinal degenerative diseases are major causes of vision loss and blindness worldwide and are characterized by chronic and progressive neuronal loss. One common feature of retinal degenerative diseases and brain neurodegenerative diseases is chronic neuroinflammation. There is growing evidence that retinal microglia, as in the brain, become activated in the course of retinal degenerative diseases, having a pivotal role in the initiation and propagation of the neurodegenerative process. A better understanding of the events elicited and mediated by retinal microglia will contribute to the clarification of disease etiology and might open new avenues for potential therapeutic interventions. This review aims at giving an overview of the roles of microgliamediated neuroinflammation in major retinal degenerative diseases like glaucoma, age-related macular degeneration, and diabetic retinopathy.

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Neurodegeneration of the retina in mouse models of Alzheimer’s disease: what can we learn from the retina?

Cited by 85 publications

References 112 publications

Alzheimer’s Disease in the Retina: Imaging Retinal Aβ Plaques for Early Diagnosis and Therapy Assessment

Alzheimer’s Disease in the Retina: Imaging Retinal Aβ Plaques for Early Diagnosis and Therapy Assessment

Macular Thickness in Subjective Memory Complaints and Mild Cognitive Impairment: A Non-Invasive Biomarker

Contribution of microglia‐mediated neuroinflammation to retinal degenerative diseases

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