The fMRI and DTI results confirmed decreased connectivity from both the PCC and hippocampus to the whole brain in MCI and AD and reduction in connectivity between these two regions, which plausibly represents an early imaging biomarker for AD.

SUMMARY Tbe complications associated with lumbar puncture (LP) were compared in 2 groups of 342 patients. The first group of patients was anticoagulated after tbe LP, and the second was not. The incidence of minor headache or back pain was similar in tbe 2 groups (Group 1-62%, Group 2-64%). Tbe anticoagulated patients had a higher incidence of paraparesis (Group 1,5 patients, Group 2, No patients;p < .05) and severe back or lumbosacral radlcular pain lasting more than 48 hours (Group 1,18 patients, Group 2,6 patients; p < . SEVERAL REPORTS have suggested that lumbar puncture (LP) followed by anticoagulation will increase the risk of spinal hemorrhage. 110 In this retrospective study we examined the risk that anticoagulation confers on LP, and identified factors which modified this risk. Methods

Recent data suggesting complex I dysfunction in Parkinson's disease (PD) arises from mitochondrial DNA (mtDNA) mutation does not conclusively answer whether the responsible genetic lesion is inherited (primary) or somatic (secondary). To address this question, we identified a family in which multiple members over three generations are affected with PD through exclusively maternal lines. Cytoplasmic hybrids (cybrids) were created for 15 family members over two generations by transferring each individual's mtDNA to mtDNA-depleted human neuroblastoma cells. Eight of the 15 cybrid lines contained mtDNA obtained from maternally descended family members and seven contained mtDNA from paternally descended family members. After 6 weeks of culture, cybrid cell lines were assayed for complex I activity and oxidative stress, and mitochondrial morphology was analyzed by electron microscopy. Compared with the cybrid lines containing mtDNA from paternal descendants, cybrid lines containing mtDNA from maternal descendants had lower complex I activity, increased reactive oxygen species production, increased radical scavenging enzyme activities, and more abnormal mitochondrial morphologic features. These findings were present in cybrid lines containing mtDNA from maternal descendants with PD as well as in currently asymptomatic young maternal descendants, and support a precedent for inherited mtDNA mutation in some persons with PD.

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