Dean and colleagues assess associations between hallmark Alzheimer disease (AD) pathology and novel quantitative neuroimaging markers while being sensitive to white matter myelin content. Widespread age-related changes to myelin were observed across the brain, particularly in late myelinating brain regions such as frontal white matter and the genu of the corpus callosum. These findings suggest amyloid pathologies significantly influence white matter and that these abnormalities may signify an early feature of the disease process. Editorial perspective is provided by Gene E. Alexander, PhD.
Finke et al study cognitive outcome and structural magnetic resonance imaging alterations in patients with anti–leucine-rich, glioma-inactivated 1 (LGI1) encephalitis. Patients with anti-LGI1 encephalitis had incomplete recovery with significant and persisting verbal (mean [SE] Rey Auditory Verbal Learning Test, delayed recall: patients, 6.52 [1.05]; controls, 11.78 [0.56], P < .001) and visuospatial (Rey-Osterrieth Complex Figure Test, delayed recall: patients, 16.0 [1.96]; controls, 25.86 [1.24]; P < .001) memory deficits. They found that anti-LGI1 encephalitis is associated with cognitive deficits and disability as a result of structural damage to the hippocampal memory system. This damage might be prevented by early immunotherapy. Editorial perspective is provided by Gregory S. Day, MD, MSc, FRCPC.
Coughlin and coauthors measure translocator protein 18 kDa (TSPO), a marker of activated glial cell response, in a cohort of National Football League (NFL) players and control participants, and report measures of white matter integrity. Using [11C]DPA-713 positron emission tomographic data from 12 active or former NFL players and 11 matched control participants, they showed that the NFL players had a higher total distribution volume in 8 of the 12 brain regions examined (P < .004). The results suggest that localized brain injury and repair, indicated by higher TSPO signal and white matter changes, may be associated with NFL play. Editorial perspective is provided by Kristina G. Witcher, BA, and Jonathan P. Godbout, PhD.
Zurawski and colleagues indicate that cortical atrophy and demyelination along the subpial surface appear early in the disease course in patients with multiple sclerosis (MS) but accelerate in progressive stages. Recent magnetic resonance imaging (MRI) data demonstrate the ability to detect such inflammation using high-resolution gadolinium-enhanced contrast scans by the presence of leptomeningeal enhancement. A growing body of evidence suggests that gray matter demyelination, cortical atrophy, and leptomeningeal inflammation may be important components of progressive MS pathology and may provide a new therapeutic target.
Highlights. JAMA Neurol. 2017;74(1):5. doi:10.1001/jamaneurol.2016.3974