Rescuing axons from degeneration does not affect retinal ganglion cell death

Lima, Silmara de; Mietto, Bruno Siqueira; Paula, Claudio Antonio; Muniz, Tiago Silva Alves; Martínez, Ana Maria Blanco; Gardino, P.F.

doi:10.1590/1414-431x20155106

Cited by 4 publications

(1 citation statement)

References 38 publications

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“…One of the main triggers of Wallerian degeneration in AD is the disruption and/or blockage of anterograde fast axonal transport [ 55 ]. Eventually impaired axonal transport leads to axonal dysregulation and increased intracellular calcium concentration activating the calcium-dependent cysteine protease calpain that mediates cytoskeletal breakdown, demyelination and axonal fragmentation [ 12 , 13 , 39 ].…”

Section: Introductionmentioning

confidence: 99%

Parietal white matter lesions in Alzheimer’s disease are associated with cortical neurodegenerative pathology, but not with small vessel disease

et al. 2017

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Cerebral white matter lesions (WML) encompass axonal loss and demyelination, and the pathogenesis is assumed to be small vessel disease (SVD)-related ischemia. However, WML may also result from the activation of Wallerian degeneration as a consequence of cortical Alzheimer’s disease (AD) pathology, i.e. hyperphosphorylated tau (HPτ) and amyloid-beta (Aβ) deposition. WML seen in AD have a posterior predominance compared to non-demented individuals but it is unclear whether the pathological and molecular signatures of WML differ between these two groups. We investigated differences in the composition and aetiology of parietal WML from AD and non-demented controls. Parietal WML tissue from 55 human post-mortem brains (AD, n = 27; non-demented controls, n = 28) were quantitatively assessed for axonal loss and demyelination, as well as for cortical HPτ and Aβ burden and SVD. Biochemical assessment included Wallerian degeneration protease calpain and the myelin-associated glycoprotein (MAG) to proteolipid protein (PLP) ratio (MAG:PLP) as a measure of hypoperfusion. WML severity was associated with both axonal loss and demyelination in AD, but only with demyelination in controls. Calpain was significantly increased in WML tissue in AD, whereas MAG:PLP was significantly reduced in controls. Calpain levels were associated with increasing amounts of cortical AD-pathology but not SVD. We conclude that parietal WML seen in AD differ in their pathological composition and aetiology compared to WML seen in aged controls: WML seen in AD may be associated with Wallerian degeneration that is triggered by cortical AD-pathology, whereas WML in aged controls are due to ischaemia. Hence, parietal WML as seen on MRI should not invariably be interpreted as a surrogate biomarker for SVD as they may be indicative of cortical AD-pathology, and therefore, AD should also be considered as the main underlying cause for cognitive impairment in cases with parietal WML.Electronic supplementary materialThe online version of this article (doi:10.1007/s00401-017-1738-2) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Parietal white matter lesions in Alzheimer’s disease are associated with cortical neurodegenerative pathology, but not with small vessel disease

et al. 2017

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Endogenous and synthetic cannabinoids induce the downregulation of cannabinoid CB1 receptor in retina

Papadogkonaki

Theodorakis

Thermos

2019

Experimental Eye Research

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Patterns of Retinal Ganglion Cell Damage in Nonarteritic Anterior Ischemic Optic Neuropathy Assessed by Swept-Source Optical Coherence Tomography

Jiang

Wang²,

Chen³

et al. 2020

Journal of Neuro-Ophthalmology

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Objective: To evaluate the ability of macular ganglion cell and inner plexiform layer (mGCIPL) and retinal nerve fiber layer (RNFL) thickness measurements by long-wavelength swept-source optical coherence tomography (SS-OCT) to assess retinal ganglion cell (RGC) damage in nonarteritic anterior ischemic optic neuropathy (NAION). Methods: A retrospective study of 20 patients with unilateral NAION was performed. SS-OCT scanning of the macular and peripapillary areas was performed to measure the total and six-sector thicknesses of macular RNFL (mRNFL) and mGCIPL, as well as peripapillary RNFL (pRNFL) thicknesses in global and 12 clock-hour sectors. Further comparison of these thicknesses between NAION involved eyes and uninvolved counterparts was performed in 12 of the 20 patients at 4 visits. The thickness map and en face images generated by volume data of the posterior pole over a 12 × 9-mm area were used for RNFL analysis. Results: Median time intervals between the visual symptom onset and first thinning occurrences of mGCIPL, mRNFL, and pRNFL were 17 days (95% Confidence Interval [CI] 14–18 days), 43 days (95% CI 32–48 days), and 70 days (95% CI 62–80 days), respectively. The thickness map indicated a significantly reduced pRNFL in the superior temporal sectors or temporal sectors after 9 weeks, and retinal damage corresponded to the superior hemisphere's mRNFL and mGCIPL. En face images showed that the RNFL thinning area gradually expanded along the retinal nerve fiber direction and progressed toward the optic nerve head. Conclusions: The patterns of RGC damage in the macular and peripapillary areas of NAION eyes can be revealed by SS-OCT. Objective measurement of SS-OCT is valuable in characterizing NAION.

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Rescuing axons from degeneration does not affect retinal ganglion cell death

Cited by 4 publications

References 38 publications

Parietal white matter lesions in Alzheimer’s disease are associated with cortical neurodegenerative pathology, but not with small vessel disease

Parietal white matter lesions in Alzheimer’s disease are associated with cortical neurodegenerative pathology, but not with small vessel disease

Endogenous and synthetic cannabinoids induce the downregulation of cannabinoid CB1 receptor in retina

Patterns of Retinal Ganglion Cell Damage in Nonarteritic Anterior Ischemic Optic Neuropathy Assessed by Swept-Source Optical Coherence Tomography

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