While various hypotheses surrounding the etiology of Alzheimer's disease (AD) have waxed and waned over the years, the calcium hypothesis of aging [1] has maintained its steady trajectory since the… Click to show full abstract
While various hypotheses surrounding the etiology of Alzheimer's disease (AD) have waxed and waned over the years, the calcium hypothesis of aging [1] has maintained its steady trajectory since the early 1990's, albeit often as the understudy. Here, Yao et al., [2] further implicate intracellular calcium dysregulation in AD pathogenesis, and focus the spotlight on the elusive ryanodine receptor-2 isoform.
               
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