A significant increase in hyperphosphorylated tau proteins (P-tau) in CSF has been shown in Alzheimer disease (AD), suggesting potential utility as biologic markers of AD. 1 Different subtypes of P-tau proteins perform differently in the discrimination of primary dementia disorders from AD. 2 Recently, we have shown that tau phosphorylated at threonine 231 (P-tau 231P ) correlates with cognitive decline in subjects with mild cognitive impairment (MCI), 3 a group at risk for AD. 4 Here, we examined in an exploratory study whether different P-tau epitopes differ in their accuracy to predict cognitive deterioration within subjects with MCI. Therefore, previously published results on P-tau 231P are again presented briefly for comparison. Moreover, we wished to know whether a combination of different P-tau epitopes is superior to a single P-tau marker for the prediction of cognitive decline.Three P-tau subtypes were measured at baseline in 59 patients with MCI. 4 Clinical follow-up was performed in all patients (mean interval 12.27 months, range 6 to 42 months). The mean (SD) age of the MCI patients (28 female) was 72.56 (7.6) years with a mean Mini-Mental State Examination (MMSE) score of 28.0 (1.9). There were 23 healthy control subjects (HC; 14 female; age 60.0 Ϯ 10.1 years; MMSE 29.2 Ϯ 0.7 points). Study subjects were recruited at two centers (Department of Psychiatry, Ludwig Maximilian University, Munich, Germany, and Department of Clinical Neuroscience, Göteborg, Sweden). P-Tau epitopes including P-tau 231P , tau protein phosphorylated at threonine 181 (P-tau 181P ), and serine 199 (P-tau 199P ) were measured using ELISAs. 2,3 Prediction of annual rate of cognitive decline (measured by MMSE change) was tested for each P-tau epitope in a separate multiple linear regression model. With use of a forward selection method, for each model, age, gender, MMSE at baseline, duration of interval, center, treatment with cognitive enhancers, and the baseline level of the respective P-tau epitope were entered as variables. A variable was entered into the model if the p value

To better define electrophysiological abnormalities in myasthenia gravis (MG) patients with muscle-specific tyrosine kinase (MuSK) antibodies (Ab), we compared electrophysiological features of 14 MuSK Ab-positive, 73 acetylcholine receptor antibody (AChR Ab)-positive, and 22 MuSK and AChR Ab-negative (seronegative) patients with generalized disease. Repetitive nerve stimulation (RNS) abnormalities were observed in 86% of MuSK Ab-positive and 82% of AChR Ab-positive patients but in only 55% of seronegative patients. RNS decrements in the orbicularis oculi were more common and severe in the MuSK Ab-positive patients than the other two groups. Single-fiber electromyography (SFEMG) of the extensor digitorum communis was abnormal in 90% of MuSK Ab-positive patients. The high frequency of RNS abnormalities in facial muscles in the MuSK Abpositive population reflects the propensity for facial muscle involvement in this form of MG and emphasizes the importance of including facial muscles in RNS protocols when evaluating these patients.

Demographic, clinical, and laboratory features were compared in 235 white and African-American (AA) patients with myasthenia gravis (MG) at the University of Alabama at Birmingham Neuromuscular Disease Clinic from May 2003 to January 2008. Seventy nine percent of patients were white. Acetylcholine receptor antibody was positive in 71% of white patients and in 59% of AA. In patients with seronegative generalized MG, the rate of positive muscle-specific tyrosine kinase antibody (MuSK-Ab) was significantly higher in AA than it was in whites (50% in AA vs. 17% in whites). Ocular MG was seronegative in 75% of AA patients. In AA, MG occurred earlier and more frequently in females, whereas, in whites, disease onset was later and more common in males. Another significant difference was a higher percentage of abnormality on repetitive nerve stimulation in AA. There was also a tendency for more severe forms of MG in AA. There are racial differences in MG between whites and AA in Alabama. These racial differences highlight the need to study biological factors in the pathogenesis of MG and to assess different approaches in diagnosis and treatment.

The authors performed nerve conduction studies in nine PARK2 and eight idiopathic Parkinson disease patients and found a significant reduction of sural sensory nerve action potential (SNAP) amplitude in eight PARK2 patients who mostly remained asymptomatic. These data suggest that sensory axonal neuropathy may be a common clinical feature of PARK2 and a reduced amplitude of sural SNAP could be a diagnostic indicator of PARK2.