Both field and laboratory studies demonstrate that hummingbirds (Apodiformes, Trochilidae) have exceptional spatial memory. The complexity of spatial-temporal information that hummingbirds must retain and use daily is probably subserved by the hippocampal formation (HF), and therefore, hummingbirds should have a greatly expanded HF. Here, we compare the relative size of the HF in several hummingbird species with that of other birds. Our analyses reveal that the HF in hummingbirds is significantly larger, relative to telencephalic volume, than any bird examined to date. When expressed as a percentage of telencephalic volume, the hummingbird HF is two to five times larger than that of caching and non-caching songbirds, seabirds and woodpeckers. This HF expansion in hummingbirds probably underlies their ability to remember the location, distribution and nectar content of flowers, but more detailed analyses are required to determine the extent to which this arises from an expansion of HF or a decrease in size of other brain regions.

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OBJECTIVES To examine associations of inflammation with physical function and potential mediation by white matter hyperintensities (WMH) in African-Americans (AA) and European-Americans (EA). DESIGN Cross-sectional analysis using linear and logistic models with Generalized Estimating Equations to account for familial clustering, reporting results as regression coefficients (β) and odds ratios (OR) adjusted for education, alcohol, exercise, BMI, hypertension, diabetes, heart disease, cognition, ankle brachial index, race-site and supported interactions. SETTING Genetic Epidemiology Network of Arteriopathy-Genetics of Microangiopathic Brain Injury Study cohort. PARTICIPANTS AA and EA sibships, ≥2 siblings with hypertension before age 60 (n=1960; 65% female, 51% AA, age 26–91y, 50% obese, 72% hypertensive). MEASUREMENTS Inflammation C-reactive protein (CRP), interleukin-6 (IL6), soluble tumor necrosis factor receptors [sTNFR] 1 and 2; magnetic resonance imaged WMH volumes (cm3). Walking speed (cm/second) over 25 feet and mobility difficulty (any self-reported difficulty walking ½ mile). RESULTS In separate models, inflammatory markers were associated with walking speed (sTNFR1: β=−2.74, p<.001; sTNFR2: −1.23, p=.03; CRP β=−1.95, p=.001; IL6 β=−1.24, p=.03) and mobility difficulty (sTNFR1: OR=1.36, p=.001; sTNFR2:OR=1.25, p=.005; CRP OR=1.22, p=.005; IL6 OR=1.18, p=.02); WMH was associated marginally only with sTNFR1 in AA (β=0.07, p=0.06). WMH were associated with walking speed in AA (AA: (β=−3.17, p=0.017; EA: β=−2.23, p=0.17) but not with mobility difficulty (OR=1.10, p=.54). Adjusting for WMH did not change associations. CONCLUSION In young-to-old persons with prevalent cardiovascular risk factors, multiple inflammatory biomarkers were associated with slower walking speed independent of microvascular disease in the brain. There was little evidence for mediation by brain WMH. Inflammation may contribute to physical function impairments through pathways other than brain microvascular disease, particularly in AA.

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