A "Calcium Hypothesis" of Declining Vision With Age

Researchers here propose that a mechanism associated with age-related cognitive decline is also involved in the poorly understood general declines in vision that occur with age. From the perspective of SENS and aging as damage, this is exactly the sort of thing we'd expect to be a secondary consequence of one of the fundamental changes that drive aging, such as a build up of aggregates or damage to cell mitochondria. Given the complexities of metabolism and cellular operation, the fastest and most efficient way to prove or disprove that - and many similar propositions - is to implement SENS and fix the underlying damage.

Extensive research in the CA1 region of the rat hippocampus has revealed an age-related increase in neuronal Ca2+ influx though L-type voltage-gated calcium channels (L-VGCCs) that is strongly linked with impaired synaptic plasticity and reduced cognitive function.

Diminished visual performance is another important behaviorally-evident functional decline that occurs with aging, beginning in young adulthood, but whose underlying mechanisms are poorly understood. Concurrent declines in neuroretinal function, when measured by electroretinogram (ERG), have also been noted: rod sensitivity and the maximum amplitude of rod responses to light both decrease with age. However, [such] physiological changes were too modest to account for the age-related vision declines. Here, we test an alternative hypothesis: that changes in retinal ion influx via L-VGCCs occur with age, and are linked to visual performance declines.

In Long-Evans rats we find a significant age-related increase in ion flux through retinal L-VGCCs in vivo [that] are longitudinally linked with progressive vision declines. Importantly, the degree of retinal Mn2+ uptake early in adulthood significantly predicted later visual contrast sensitivity declines. Furthermore, as in the aging hippocampus, retinal expression of a drug-insensitive L-VGCC isoform (α1D) increased - a pattern confirmed in vivo by an age-related decline in sensitivity to L-VGCC blockade. These data highlight mechanistic similarities between retinal and hippocampal aging, and raise the possibility of new treatment targets for minimizing vision loss during healthy aging.

Link: http://dx.doi.org/10.1371/journal.pone.0056340


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