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2017 ; 12
(4
): 538-548
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The complexities underlying age-related macular degeneration: could amyloid beta
play an important role?
#MMPMID28553324
Lynn SA
; Keeling E
; Munday R
; Gabha G
; Griffiths H
; Lotery AJ
; Ratnayaka JA
Neural Regen Res
2017[Apr]; 12
(4
): 538-548
PMID28553324
show ga
Age-related macular degeneration (AMD) causes irreversible loss of central vision
for which there is no effective treatment. Incipient pathology is thought to
occur in the retina for many years before AMD manifests from midlife onwards to
affect a large proportion of the elderly. Although genetic as well as
non-genetic/environmental risks are recognized, its complex aetiology makes it
difficult to identify susceptibility, or indeed what type of AMD develops or how
quickly it progresses in different individuals. Here we summarize the literature
describing how the Alzheimer's-linked amyloid beta (A?) group of misfolding
proteins accumulate in the retina. The discovery of this key driver of
Alzheimer's disease in the senescent retina was unexpected and surprising,
enabling an altogether different perspective of AMD. We argue that A?
fundamentally differs from other substances which accumulate in the ageing
retina, and discuss our latest findings from a mouse model in which physiological
amounts of A? were subretinally-injected to recapitulate salient features of
early AMD within a short period. Our discoveries as well as those of others
suggest the pattern of A? accumulation and pathology in donor aged/AMD tissues
are closely reproduced in mice, including late-stage AMD phenotypes, which makes
them highly attractive to study dynamic aspects of A?-mediated retinopathy.
Furthermore, we discuss our findings revealing how A? behaves at single-cell
resolution, and consider the long-term implications for neuroretinal function. We
propose A? as a key element in switching to a diseased retinal phenotype, which
is now being used as a biomarker for late-stage AMD.
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