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In This Issue of JAMA Neurology |

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JAMA Neurol. 2013;70(11):1337-1339. doi:10.1001/jamaneurol.2013.2892.
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Butcher and coauthors evaluate a possible association between 22q11.2 deletions and Parkinson disease. Shulman provides editorial perspective.

Related Editorial

Veiby and colleagues determine whether signs of impaired development appear already during the first months of life in children exposed prenatally to antiepileptic drugs, and they explore potential adverse effects of antiepileptic drug exposure through breastfeeding. Van Ness provides commentary in a related editorial.

Related Editorial

Kitley et al assess if AQP4-Ab–negative patients with longitudinally extensive transverse myelitis share similar disease characteristics with AQP4-Ab–positive patients or whether they have distinct features and alternative diagnoses.

Marder and colleagues determine whether the MeDi modifies the time to clinical onset of Huntington disease (phenoconversion) in premanifest carriers participating in Prospective Huntington at Risk Observational Study (PHAROS) and to examine the effects of body mass index and caloric intake on time to phenoconversion.

Fletcher and coauthors examine the involvement of the hippocampus-fornix circuit in the very earliest stages of cognitive impairment and determine whether the volumes of fornix white matter and hippocampal gray matter would be useful markers for understanding the onset of dementia and for clinical intervention.

Savica et al investigate the incidence of dementia with Lewy bodies among residents of Olmsted County, Minnesota, and compare it with the incidence of Parkinson disease dementia.

Le Ber and colleagues evaluate the exact contribution of SQSTM1 to frontotemporal dementia (FTD) and frontotemporal dementia with amyotrophic lateral sclerosis (FTD-ALS) in an independent cohort of French patients.

Wood and coauthors ascertain the frequency of inherited frontotemporal lobar degeneration and develop a validated pedigree classification criteria.

Wilson et al conduct a longitudinal clinical-pathologic cohort study to test the hypothesis that transactive response DNA-binding protein 43 (TDP-43) is related to late-life cognitive decline.


Leen and colleagues determine the value of cerebrospinal fluid analysis in the workup for GLUT1 deficiency syndrome.





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