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This Month in Archives of Neurology
Arch Neurol. 2009;66(5):552-553.
The Mirror Neuron System
Cattaneo and Rizzolatti (SEE ARTICLE) have discovered a class of neurons in the premotor cortex of monkeys that discharge both when individuals perform a given motor act and when they observe the same motor act performed by others. Ample evidence demonstrates the existence in humans of a cortical network with the properties of mirror neurons (mirror system). The human mirror system is involved in understanding the actions of others and the intentions behind them, and it underlies mechanisms of observational learning. Clinical implications of the mirror system are discussed.
Pramipexole vs Levodopa in Early Parkinson Disease
The Parkinson Study Group CALM (Comparison of the Agonist Pramipexole With Levodopa on Motor Complications) Cohort Investigators (SEE ARTICLE) describe persistent differences favoring initial pramipexole in the rates of dopaminergic motor complications, with less severe somnolence favoring initial levodopa.
Mutations for Gaucher Disease Increase the Risk for Parkinson Disease
Mitsui and colleagues (SEE ARTICLE) show that heterozygous pathogenic variants in the glucocerebrosidase gene confer an increased risk for sporadic Parkinson disease. Editorial perspective is provided by James B. Leverenz, MD, Oscar L. Lopez, MD, and Steven T. DeKosky, MD. (SEE ARTICLE)
Glucocerebrosidase Mutations Are Associated With Dementia With Lewy Bodies
Clark et al (SEE ARTICLE) report that glucocerebrosidase gene mutations are associated with Lewy body disorders with extensive (cortical) Lewy bodies and may be a useful marker for Lewy body disorders. Editorial perspective is provided by James B. Leverenz, MD, Oscar L. Lopez, MD, and Steven T. DeKosky, MD. (SEE ARTICLE)
A Single, Early Magnetic Resonance Imaging Scan for Diagnosing Multiple Sclerosis
Rovira and colleagues (SEE ARTICLE) find that a single brain magnetic resonance image demonstrates dissemination in space and shows both gadolinium-enhancing and -nonenhancing lesions, suggesting that dissemination in time is highly specific for predicting the early development of clinically definite multiple sclerosis, even when the scan is performed in the first 3 months after the onset of a clinically isolated syndrome.
Comparing Progressive Multifocal Leukoencephalopathy and Relapsing-Remitting Multiple Sclerosis
Boster et al (SEE ARTICLE) indicate that there are differences between the clinical and magnetic resonance imaging characteristics of progressive multifocal leukoencephalopathy (PML) and relapsing-remitting multiple sclerosis, which may help distinguish new multiple sclerosis activity from PML. Brain magnetization transfer ratio studies may provide additional clues to improve early detection of PML in patients with preexisting multiple sclerosis and warrant further study.
Abnormal White Matter in Multiple Sclerosis
Seewann and colleagues (SEE ARTICLE) classify diffusely abnormal white matter (DAWM) in chronic multiple sclerosis as a pathology that is different from normal-appearing white matter and focal white matter lesions, most likely resulting from the cumulative effect of ongoing inflammation and axonal pathology. Thus, DAWM is likely to contribute to disease progression and may prove to be an important new disease marker in clinical trials.
Prior Stroke With Cognitive Function and Impairment
Knopman et al (SEE ARTICLE) report that in a population-based sample of nondemented persons, a history of stroke was particularly associated with nonamnestic mild cognitive impairment and with impairment in nonmemory cognition. The APOE  4 genotype was associated with memory impairment and amnestic mild cognitive impairment.
The Anesthetic Sevoflurane Induces Apoptosis and Increases β-Amyloid Levels
Dong and colleagues (SEE ARTICLE) indicate that the inhalational anesthetic sevoflurane may promote Alzheimer disease neuropathogenesis. If confirmed in humans, it may be prudent to caution against the use of sevoflurane as an anesthetic, especially in those suspected of possessing excessive levels of cerebral β-amyloid.
Preclinical Evidence of Alzheimer Changes: CSF Biomarker and Positron Emission Tomographic Findings
Petrie et al (SEE ARTICLE) show that in healthy individuals, higher cerebrospinal fluid (CSF) tau and phosphorylated tau 181 concentrations were associated with more severe hypometabolism in several brain regions affected early in Alzheimer disease, while lower CSF Aβ42 concentrations were associated with hypometabolism only in the medial temporal lobe.
Cerebrospinal Fluid Biomarkers Predict Rate of Cognitive Decline in Alzheimer Disease
Snider and colleagues (SEE ARTICLE) report that in individuals with very mild dementia of the Alzheimer type, lower cerebrospinal fluid levels of β-amyloid (Aβ) 42, high tau or phosphorylated tau 181, or a high tau to Aβ42 ratio quantitatively predict more rapid progression of cognitive deficits and dementia.
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Changes in Clinical Dementia Rating sum of boxes (CDR-SB) scores across time. A, Data for the 10 individuals with the lowest cerebrospinal fluid (CSF) Aβ peptide 1-42 (Aβ42) levels (182-263 pg/mL). Each data point is the CDR-SB score from the clinical assessment at the indicated time relative to the lumbar puncture (LP) (time 0). B, Data for the 10 individuals with the highest CSF Aβ42 levels (588-1179 pg/mL). The timing of the baseline LP was set at time "0" (dotted line). All the participants had a global CDR of 0.5 (with a CDR-SB score of 0.5-4.5) at the assessment before the LP.
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Cortical  7 Nicotinic Receptor and β-Amyloid Levels in Alzheimer Disease
Ikonomovic et al (SEE ARTICLE) indicate that during the clinical progression from normal cognition to neurodegenerative disease state, total β-amyloid peptide concentration increases, while  7 nicotinic acetylcholine receptors remain relatively stable in the superior frontal cortex. Thus, these data support the hypothesis that cellular expression of these receptors may be upregulated selectively in β-amyloid plaque–burdened brain areas.
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