Age-related decrease in rod bipolar cell density of the human retina: an immunohistochemical study

Aggarwal, P; Nag, Tapas Chandra; Wadhwa, Shashi

doi:10.1007/s12038-007-0029-9

Cited by 48 publications

(44 citation statements)

References 20 publications

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“…Klein et al16 found that in a control group of subjects, arteriolar caliber decreased by 1.0 m/decade and venular caliber decreased by 0.7 m/decade. Retinal cell number has also been reported to decrease with age 17,18,19,20. Harman et al17 found a decrease in neuron number in the retinal ganglion cell layer with increasing age; they estimated that in the macular region, neuronal density decreased by 0.29% per year.…”

Section: Discussionmentioning

confidence: 99%

“…Bipolar cells may also be involved in retinal thinning. Aggarwal et al20 found that after the third decade, rod bipolar cell density starts to decrease. From our analysis we cannot ascertain the source of the retinal thinning not accounted for by loss of RNFL; however, it is likely due to a combination of decreases in vessel caliber and loss of retinal ganglion, photoreceptor, bipolar, and RPE cells.…”

Section: Discussionmentioning

confidence: 99%

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OCT Reveals Regional Differences in Macular Thickness with Age

Neuville

Bronson-Castain²,

Bearse³

et al. 2009

Optometry and Vision Science

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Purpose In order to assist identification of macular thickness abnormalities by optical coherence tomography (OCT), we use techniques that improve spatial localization across the retina to establish any age-related retinal thickness changes in healthy eyes. Methods Retinal thickness was measured in 30 eyes of 30 healthy subjects aged 13–69 years. Using Stratus OCT™ 3, twelve radial scans centered at the foveola were acquired and points between scans were interpolated to create a topographic map of the central 20°. The thickness map was divided into 37 hexagonal regions. A mean retinal thickness for each hexagon was computed. Retinal thickness versus age was evaluated for the entire scanned area, 5 anatomical regions, and within individual hexagons. The retinal nerve fiber layer (RNFL) contribution to total retinal thinning was analyzed in the papillomacular region. Results There was a small but significant thinning of the overall macular area with increasing age (2.7 μm/decade; P = 0.027). Comparing the 10 youngest subjects (age 13–27) to the 10 oldest (age 51–68), retinal thicknesses in the temporal, superior, inferior and foveal regions were not significantly different. However, the two age groups differed significantly in retinal thickness in the nasal region (P < 0.008). Across all subjects retinal thickness in this region was linearly correlated with age, decreasing by 4.1μm/decade (P < 0.002). Approximately 43% of the retinal thinning in the nasal region was attributed to RNFL loss. Conclusions The method of OCT acquisition and analysis used in this study allows for greater spatial localization of change in retinal thickness due to age or pathological processes. Based on the results of this study, the macula thins with increasing age, but does so non-uniformly. The greatest amount of thinning occurs nasal to the fovea. RNFL loss accounts for much, but not all of, the thinning in this area.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

OCT Reveals Regional Differences in Macular Thickness with Age

Neuville

Bronson-Castain²,

Bearse³

et al. 2009

Optometry and Vision Science

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“…Recent studies in mice and humans have shown that a normally aging retina goes through pathological changes including the formation of ectopic photoreceptor synapses, increased inflammation, and gradual photoreceptor cell degeneration (Aggarwal et al 2007, Eliasieh et al 2007, Fuchs et al 2012, Samuel et al 2011, Terzibasi et al 2009). Similar retinal abnormalities have been observed in retinal degenerative diseases such as age-related macular degeneration (AMD) (Aggarwal et al 2007, Eliasieh et al 2007, Sullivan et al 2007), suggesting a link between the molecular mechanisms of retinal aging and age-dependent retinal diseases. Elucidating the molecular mechanisms causing these age-dependent retinal abnormalities will enhance our understanding of the molecular and cellular changes underlying aging and age-dependent diseases in the retina.…”

Section: Introductionmentioning

confidence: 99%

Genetic basis of age-dependent synaptic abnormalities in the retina

et al. 2014

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Understanding the normal aging process will help us determine the mechanisms of how age-related diseases are caused and progress. A/J inbred mice have been shown to exhibit accelerated aging phenotypes in the retina including increased inflammation and photoreceptor cell degeneration, which resemble human aging symptoms. C57BL/6J (B6) inbred mice are less susceptible for these abnormalities, indicating the existence of genetic factor(s) that affect their severity. In this study, we determined that another age-dependent phenotype, ectopic synapse formation, is also accelerated in the A/J retina compared to the B6 retina. Through genetic mapping utilizing recombinant inbred strains, we identified quantitative trait loci (QTLs) on chromosome 7 and 19 that contribute to abnormal retinal synapses as well as other age-dependent phenotypes. Using consomic single chromosome substitution lines where a single chromosome is from A/J and the rest of the genome is B6, we investigated the individual effect of each QTL on retinal aging phenotypes. We observed that both QTLs independently contribute to abnormal retinal synapses, reduction in the number of cone cells, and an up-regulation of retinal stress marker, glial fibrillary acidic protein (GFAP). Mice with a single chromosome substitution on chromosome 19 also exhibited an increase in inflammatory cells, which is characteristic of aging and age-related macular degeneration. Thus, we identified QTLs that are independently capable of affecting the severity and progression of age-dependent retinal abnormalities in mice.

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“…[3][4][5][6] Photoreceptors are the most numerous and metabolically active cells in the retina, with a large number of mitochondria, having high oxygen consumption. The cells of the inner nuclear layer and the ganglion cell layer represent ,10% of the number of photoreceptors, [7][8][9] and thus, additional damage to the inner retina is unlikely to significantly improve clinical efficacy. After a laser burn, the photoreceptor layer is partially replaced by glial tissue.…”

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confidence: 99%