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Qureshi and Mehler (Article) complete their 3-part series with this review in which they survey the therapeutic potential of exogenous stem cells and endogenous neural stem and progenitor cells (NSPCs). They also highlight innovative technological approaches for designing, developing, and delivering epigenetic therapies for targeted reprogramming of endogenous pools of NSPCs, neural cells at risk, and dysfunctional neural networks to rescue and restore neurological function in the ischemic brain.
Fueyo and colleagues (Article) document therapeutic advances in the field of neuro-oncology that were made during the last decade. First, there were conceptual advances in the molecular and cell biology of malignant gliomas including the discovery in 2004 of brain tumor stem cells. Second, the Cancer Genome Atlas project has been extremely useful in the discovery of new molecular markers, including mutations in the IDH1 gene, and has led to a new classification of gliomas based on the differentiation status and mesenchymal transformation. In addition, use of the 1p/19q marker and O6-methylguanine-DNA methyltransferase methylation status have been identified as guides for patient selection for therapies and represent the first steps toward personalized medicine for treating gliomas. Finally, progress has been made in treatment strategies including the establishment of temozolomide as the criterion standard for treating gliomas, the adoption of bevacizumab in the clinical setting, and developments in experimental biological therapies including cancer vaccines and oncolytic adenoviruses.
Langer-Gould et al (Article) determine whether low levels of 25-hydroxyvitamin D (25[OH]D) contribute to the increased risk of postpartum multiple sclerosis (MS) relapses. They report that pregnancy and exclusive breastfeeding are strongly associated with low 25(OH)D levels in women with MS. However, these lower vitamin D levels were not associated with an increased risk of postpartum MS relapses. These data suggest that a low level of vitamin D in isolation is not an important risk factor for postpartum MS relapses.
Mean (SD) 25-hydroxyvitamin D (serum 25[OH]D) levels in women who had postpartum multiple sclerosis relapses (n = 12) and women with multiple sclerosis who were relapse-free during pregnancy and the first 6 months after childbirth (n = 16), during the third trimester of pregnancy, and the postpartum period. * P = .04, unadjusted; P = .04, adjusted for season. To convert 25(OH)D to nanomoles per liter, multiply by 2.496.
Evatt and colleagues (Article) examine the prevalence of vitamin D insufficiency in a cohort of untreated patients with early Parkinson disease (PD) (diagnosed within 5 years of study entry). They find that the prevalence of vitamin D insufficiency in patients with early-stage PD was similar to or higher than those reported in previous studies. Vitamin D concentrations did not decrease during progression of PD. They recommend that further studies are needed to elucidate the natural history and significance of vitamin D insufficiency in PD.
Lee and colleagues (Article) identify novel loci for late-onset Alzheimer disease (LOAD) in Caribbean Hispanic individuals and replicate the findings in a publicly available data set from the National Institute on Aging Late-Onset Alzheimer Disease Family Study. Their genome-wide search of Caribbean Hispanic individuals identified several novel genetic variants associated with LOAD and replicated these associations in a white cohort. They also replicated associations in CLU, PICALM, and BIN1 in the Caribbean Hispanic cohort.
Womack et al (Article) evaluate the cause of diagnostic errors in the visual interpretation of positron emission tomographic scans with fludeoxyglucose F18 (FDG-PET) in patients with frontotemporal lobar degeneration (FTLD) and patients with Alzheimer disease. They report that temporoparietal hypometabolism in FTLD is common and may cause inaccurate interpretation of FDG-PET scans. The accurate interpretation of FDG-PET scans in patients with dementia cannot rest on the presence or absence of a single region of hypometabolism but rather must take into account the relative hypometabolism of all brain regions.
Vergouwen and colleagues (Article) characterize the vessel wall imaging findings and enhancement patterns in the middle cerebral artery of patients with presumed atherosclerotic disease and recent infarction in the territory of the affected artery. Their data suggest that patients with presumed intracranial atherosclerosis of the middle cerebral arteries have eccentric plaques that enhance after the administration of contrast medium when imaging is performed within weeks to months of a cerebral infarct within the arterial territory.
Okereke and colleagues (Article) develop a brief instrument for obtaining Clinical Dementia Rating (CDR) scores and to assess its reliability and cross-sectional validity. They find the Structured Interview & Scoring Tool–Massachusetts Alzheimer's Disease Research Center is a brief, reliable, and sensitive instrument for obtaining CDR scores in persons with symptoms along the spectrum of mild cognitive change.
Wilson et al (Article) characterize the course of cognitive decline during the prodromal phase of Alzheimer disease. They find that dementia due to Alzheimer disease is preceded by about 5 to 6 years of accelerated decline in multiple cognitive functions. By contrast, little decline is evident in persons not developing Alzheimer disease.
Setó-Salvia and colleagues (Article) determine whether the microtubule-associated protein tau (MAPT) H1 haplotype and MAPT subhaplotypes play a role in the risk of Parkinson disease (PD) and Parkinson disease–dementia (PDD) complex. Their data confirm that MAPT H1 is associated with PD and has a strong influence on the risk of dementia in patients with PD. Their results also suggest that none of the MAPT subhaplotypes plays a significant role in other neurodegenerative diseases, such as Lewy body dementia or Alzheimer disease.
Naunheim and colleagues (Article) present a case report of arterial tortuosity syndrome which is a rare connective tissue disorder characterized by tortuosity, dilation, stenosis, and aneurysms of large and mid-size arteries. They report a new manifestation of this rare clinical syndrome in the absence of skin and soft-tissue abnormalities, bilateral, giant, fusiform intracranial aneurysms. Editorial perspective is provided by Louis R. Caplan, MD (Article).
This Month in Archives of Neurology. Arch Neurol. 2011;68(3):290-291. doi:10.1001/archneurol.2011.12