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	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

In their recent article, Jenkins et al¹ did not find total intracranial volume (TIV) to differ significantly between subjects with Alzheimer disease (AD) and controls, and therefore their results did not support a brain reserve hypothesis or the theory that larger premorbid size is protective against AD.

The brain reserve hypothesis is intriguing because, within a number of biological systems, size does relate to complexity or redundancy, and size often represents a protective factor against aging, injury, and/or disease.^{2, 3} Brain size also relates to the complexity of cognitive tasks that can be performed by a given species,⁴ and in humans, brain size relates to psychometric intelligence.^{5, 6} Premorbid intellectual ability may relate to dementia.⁷ Ultimate cranial capacity (the indirect measure for brain size) stabilizes by adolescence and occurs as a combination of genetic, biological, and environmental influences in utero and during infant and child development. Throughout this formative period, cranial capacity . . . [Full Text of this Article]