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Melanopsin retinal ganglion cell loss in Alzheimer's disease

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Harvard

La Morgia, C, Ross-Cisneros, FN, Koronyo, Y, Hannibal, J, Gallassi, R, Cantalupo, G, Sambati, L, Pan, BX, Tozer, KR, Barboni, P, Provini, F, Avanzini, P, Carbonelli, M, Pelosi, A, Chui, H, Liguori, R, Baruzzi, A, Koronyo-Hamaoui, M, Sadun, AA & Carelli, V 2015, 'Melanopsin retinal ganglion cell loss in Alzheimer's disease' Annals of Neurology. https://doi.org/10.1002/ana.24548

APA

La Morgia, C., Ross-Cisneros, F. N., Koronyo, Y., Hannibal, J., Gallassi, R., Cantalupo, G., ... Carelli, V. (2015). Melanopsin retinal ganglion cell loss in Alzheimer's disease. Annals of Neurology. https://doi.org/10.1002/ana.24548

CBE

La Morgia C, Ross-Cisneros FN, Koronyo Y, Hannibal J, Gallassi R, Cantalupo G, Sambati L, Pan BX, Tozer KR, Barboni P, Provini F, Avanzini P, Carbonelli M, Pelosi A, Chui H, Liguori R, Baruzzi A, Koronyo-Hamaoui M, Sadun AA, Carelli V. 2015. Melanopsin retinal ganglion cell loss in Alzheimer's disease. Annals of Neurology. https://doi.org/10.1002/ana.24548

MLA

Vancouver

La Morgia C, Ross-Cisneros FN, Koronyo Y, Hannibal J, Gallassi R, Cantalupo G et al. Melanopsin retinal ganglion cell loss in Alzheimer's disease. Annals of Neurology. 2015 Oct 27. https://doi.org/10.1002/ana.24548

Author

La Morgia, Chiara ; Ross-Cisneros, Fred N ; Koronyo, Yosef ; Hannibal, Jens ; Gallassi, Roberto ; Cantalupo, Gaetano ; Sambati, Luisa ; Pan, Billy X ; Tozer, Kevin R ; Barboni, Piero ; Provini, Federica ; Avanzini, Pietro ; Carbonelli, Michele ; Pelosi, Annalisa ; Chui, Helena ; Liguori, Rocco ; Baruzzi, Agostino ; Koronyo-Hamaoui, Maya ; Sadun, Alfredo A ; Carelli, Valerio. / Melanopsin retinal ganglion cell loss in Alzheimer's disease. In: Annals of Neurology. 2015.

Bibtex

@article{92b89eff5e014869b1438ee85d14845c,
title = "Melanopsin retinal ganglion cell loss in Alzheimer's disease",
abstract = "OBJECTIVE: Melanopsin retinal ganglion cells (mRGCs) are photoreceptors driving circadian photoentrainment, and circadian dysfunction characterizes Alzheimer's disease (AD). We investigated mRGCs in AD, hypothesizing their contribution to circadian dysfunction.METHODS: We 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 co-immunostained for retinal amyloid-β (Aβ) deposition and melanopsin to locate mRGCs. All AD cohorts were compared with age-matched controls.RESULTS: We 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.INTERPRETATION: We 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. This article is protected by copyright. All rights reserved.",
author = "{La Morgia}, Chiara and Ross-Cisneros, {Fred N} and Yosef Koronyo and Jens Hannibal and Roberto Gallassi and Gaetano Cantalupo and Luisa Sambati and Pan, {Billy X} and Tozer, {Kevin R} and Piero Barboni and Federica Provini and Pietro Avanzini and Michele Carbonelli and Annalisa Pelosi and Helena Chui and Rocco Liguori and Agostino Baruzzi and Maya Koronyo-Hamaoui and Sadun, {Alfredo A} and Valerio Carelli",
note = "{\circledC} 2015 American Neurological Association.",
year = "2015",
month = "10",
day = "27",
doi = "10.1002/ana.24548",
language = "English",
journal = "Annals of Neurology",
issn = "0364-5134",
publisher = "John/Wiley & Sons, Inc. John/Wiley & Sons Ltd",

}

RIS

TY - JOUR

T1 - Melanopsin retinal ganglion cell loss in Alzheimer's disease

AU - La Morgia, Chiara

AU - Ross-Cisneros, Fred N

AU - Koronyo, Yosef

AU - Hannibal, Jens

AU - Gallassi, Roberto

AU - Cantalupo, Gaetano

AU - Sambati, Luisa

AU - Pan, Billy X

AU - Tozer, Kevin R

AU - Barboni, Piero

AU - Provini, Federica

AU - Avanzini, Pietro

AU - Carbonelli, Michele

AU - Pelosi, Annalisa

AU - Chui, Helena

AU - Liguori, Rocco

AU - Baruzzi, Agostino

AU - Koronyo-Hamaoui, Maya

AU - Sadun, Alfredo A

AU - Carelli, Valerio

N1 - © 2015 American Neurological Association.

PY - 2015/10/27

Y1 - 2015/10/27

N2 - OBJECTIVE: Melanopsin retinal ganglion cells (mRGCs) are photoreceptors driving circadian photoentrainment, and circadian dysfunction characterizes Alzheimer's disease (AD). We investigated mRGCs in AD, hypothesizing their contribution to circadian dysfunction.METHODS: We 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 co-immunostained for retinal amyloid-β (Aβ) deposition and melanopsin to locate mRGCs. All AD cohorts were compared with age-matched controls.RESULTS: We 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.INTERPRETATION: We 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. This article is protected by copyright. All rights reserved.

AB - OBJECTIVE: Melanopsin retinal ganglion cells (mRGCs) are photoreceptors driving circadian photoentrainment, and circadian dysfunction characterizes Alzheimer's disease (AD). We investigated mRGCs in AD, hypothesizing their contribution to circadian dysfunction.METHODS: We 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 co-immunostained for retinal amyloid-β (Aβ) deposition and melanopsin to locate mRGCs. All AD cohorts were compared with age-matched controls.RESULTS: We 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.INTERPRETATION: We 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. This article is protected by copyright. All rights reserved.

U2 - 10.1002/ana.24548

DO - 10.1002/ana.24548

M3 - Journal article

JO - Annals of Neurology

JF - Annals of Neurology

SN - 0364-5134

ER -

ID: 45980899