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Butz, M.

Publications and source records attributed to Butz, M..

2 recordsLinked to original sources

Slowing of Frontocentral Beta Oscillations in Atypical Parkinsonism

Diagnosis of atypical parkinsonian syndromes mostly relies on clinical presentation as well as structural and molecular brain imaging. It has not been investigated whether cortical oscillatory activity exhibits features distinguishing these syndromes. Therefore, we measured resting-state magnetoencephalography in 13 patients with corticobasal syndrome, 10 patients with progressive supranuclear palsy, 23 patients with idiopathic Parkinsons disease and 23 healthy controls. We compared spectral power as well as amplitude and frequency of power peaks between the groups. Atypical Parkinsonism was associated with spectral slowing, distinguishing both corticobasal syndrome and progressive supranuclear palsy from age-matched healthy controls and Parkinsons disease. Patients with atypical Parkinsonism showed a shift of beta peaks (13-30 Hz) towards lower frequencies in frontal and central areas bilaterally. A concomitant increase in theta/alpha power relative to controls was observed in both atypical parkinsonian syndromes and in Parkinsons disease. Our results demonstrate that slowing of frontocentral beta oscillations is characteristic of atypical Parkinsonism. Spectral slowing with a different topography has previously been observed in other neurodegenerative disorders, such as Alzheimers disease, suggesting that spectral slowing might be an electrophysiological marker of cortical neurodegeneration. As such, it might support differential diagnosis of parkinsonian syndromes in the future. HighlightsO_LISlowing of beta oscillations distinguishes atypical parkinsonian syndromes from healthy controls and idiopathic Parkinsons disease C_LIO_LISpectral slowing is most pronounced in frontocentral areas C_LIO_LIBeta oscillations are shifted towards lower frequencies independent of their amplitude C_LI

neuroscience↗

Improved RAD51 binders through motif shuffling based on the modularity of BRC repeats

Exchanges of protein sequence modules support leaps in function unavailable through point mutations during evolution. Here we study the role of the two RAD51-interacting modules within the eight binding BRC repeats of BRCA2. We created 64 chimeric repeats by shuffling these modules and measured their binding to RAD51. We found that certain shuffled repeats were stronger than any of the natural repeats, suggesting balancing of relative properties in BRC repeats. Surprisingly, the contribution from the two modules was poorly correlated with affinities of natural repeats, with weak BRC8 repeat containing the most effective N-terminal module. The binding of the strongest chimera, BRC8-2, to RAD51 was improved by -2.44 kCal/mol compared to the strongest natural repeat, BRC4. Crystal structure of RAD51:BRC8-2 complex shows an improved interface fit and an extended {beta}-hairpin in this repeat. BRC8-2 was shown to function in human cells, preventing the formation of nuclear foci after ionizing radiation.

biochemistry↗