Jack and colleagues compare age, sex, and APOE ε4 effects on memory, brain structure (adjusted hippocampal volume [HVa]), and amyloid positron emission tomography (PET) in cognitively normal individuals aged 30 to 95 years old. They studied 1246 cognitively normal individuals, including 1209 participants aged 50 to 95 years old enrolled in a population-based study of cognitive aging and 37 self-selected volunteers aged 30 to 49 years old. The HVa worsened gradually from age 30 years to the mid-60s and more steeply beyond that age. The median amyloid PET was low until age 70 years and increased thereafter. Editorial perspective is provided by Charles DeCarli, MD.
Hohman et al evaluate whether vascular endothelial growth factor (VEGF) levels are associated with brain aging outcomes (hippocampal volume and cognition) and further evaluate whether VEGF modifies relations between Alzheimer disease biomarkers and brain aging outcomes. Cerebrospinal fluid VEGF was cross-sectionally related to brain aging outcomes (hippocampal volume, episodic memory, and executive function) using a general linear model and longitudinally using mixed-effects regression. Vascular endothelial growth factor was associated with baseline hippocampal volume (t277 = 2.62; P = .009), longitudinal hippocampal atrophy (t858 = 2.48; P = .01), and longitudinal decline in memory (t1629 = 4.09; P < .001) and executive function (t1616 = 3.00; P = .003). Editorial perspective is provided by Peter T. Nelson, MD, PhD, and Gregory A. Jicha, MD, PhD.
Meier and coauthors longitudinally assess the recovery of cerebral blood flow (CBF) in a carefully selected sample of collegiate athletes and compare time course of CBF recovery with that of cognitive and behavioral symptoms. Arterial spin labeling magnetic resonance imaging was used to collect voxelwise relative CBF at each visit. Imaging data suggested both cross-sectional (ie, healthy vs concussed athletes; P < .05) and longitudinal (1 day and 1 week vs 1 month postinjury; P < .001) evidence of CBF recovery in the right insular and superior temporal cortex.
Author Audio Interview and Continuing Medical Education
Rinaldi and colleagues identify the genetic cause for a novel form of pure autosomal dominant hereditary spastic paraplegia (HSP). They examined and followed up with a family presenting to a tertiary referral center for evaluation of HSP for a decade until August 2014. They identified the nucleotide substitution c.109C>T in exon 3 of CPT1C, which determined the base substitution of an evolutionarily conserved Cys residue for an Arg in the gene product.
Highlights. JAMA Neurol. 2015;72(5):491. doi:10.1001/jamaneurol.2014.2846