The number and proportion of older adults in the community is projected to increase significantly over the coming decades. It is estimated that the global population of adults aged over 65 years will increase from 703 million in 2019 to 1.5 billion by 2050 (United Nations, 2019). The rise in the number and proportion of older people stems from declining birth and fertility rates and an increase in the average lifespan across the world (United Nations, 2019).

This review provides a qualitative and quantitative analysis of cerebral glucose metabolism in ageing. We undertook a systematic literature review followed by pooled effect size and activation likelihood estimates (ALE) meta‐analyses. Studies were retrieved from PubMed following the PRISMA guidelines. After reviewing 635 records, 21 studies with 22 independent samples ( n = 911 participants) were included in the pooled effect size analyses. Eight studies with eleven separate samples ( n = 713 participants) were included in the ALE analyses. Pooled effect sizes showed significantly lower cerebral metabolic rates of glucose for older versus younger adults for the whole brain, as well as for the frontal, temporal, parietal, and occipital lobes. Among the sub‐cortical structures, the caudate showed a lower metabolic rate among older adults. In sub‐group analyses controlling for changes in brain volume or partial volume effects, the lower glucose metabolism among older adults in the frontal lobe remained significant, whereas confidence intervals crossed zero for the other lobes and structures. The ALE identified nine clusters of lower glucose metabolism among older adults, ranging from 200 to 2640 mm 3 . The two largest clusters were in the left and right inferior frontal and superior temporal gyri and the insula. Clusters were also found in the inferior temporal junction, the anterior cingulate and caudate. Taken together, the results are consistent with research showing less efficient glucose metabolism in the ageing brain. The findings are discussed in the context of theories of cognitive ageing and are compared to those found in neurodegenerative disease.

This review provides a qualitative and quantitative analysis of cerebral glucose in ageing. We undertook a systematic review of the literature followed by pooled effect size and Activation Likelihood Estimates (ALE) meta-analyses. Studies were retrieved from PubMed following the PRISMA guidelines. After reviewing 653 records, 22 studies with 24 samples (n = 993 participants) were included in the pooled effect size analyses. Eight studies with 11 samples (n = 713 participants) were included in the ALE analyses. Pooled effect sizes showed significantly lower cerebral metabolic rates of glucose for older versus younger adults for the whole brain, as well as for the frontal, temporal, parietal and occipital lobes. Among the sub-cortical structures, the caudate showed a lower metabolic rate among older adults. In sub-group analyses controlling for changes in brain volume or partial volume effects, the lower glucose metabolism among older adults in the frontal lobe remained significant, whereas confidence intervals crossed zero for the other lobes and structures. The ALE identified nine clusters of lower glucose metabolism among older adults, ranging from 200mm3 to 2,640mm3. The two largest clusters were in the left and right inferior frontal and superior temporal gyri and the insula. Clusters were also found in the inferior temporal junction, the anterior cingulate and caudate. Taken together, the results of the meta-analyses are consistent with research showing less efficient glucose metabolism in the ageing brain. The findings are discussed in the context of theories of cognitive ageing and are compared to those found in neurodegenerative disease.

Neuroimaging methods provide a non-invasive means to understand how the brain changes over the course of a typical lifespan in-vivo. Macroscale neuroimaging studies of “healthy” human ageing rarely consider small-scale (microscale) biological processes that underlie age-related changes to the tissues, processes and functions of the brain. By considering these microscale changes, we stand to better understand the underlying causes and processes that give rise to age-related cerebral changes captured by these images. This review addresses the gap by describing the known and putative connections between neuroimaging studies of ageing and molecular biology. The connections are described in relation to structural, inflammatory, vascular, and metabolic brain changes with age. We summarise the cerebral changes, how they can be visualised with neuroimaging methods and the microscale biological processes that underlie the visible macroscale changes.