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This Month in Archives of Neurology |

This Month in Archives of Neurology FREE

Arch Neurol. 2010;67(8):914-915. doi:10.1001/archneurol.2010.171.
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NATALIZUMAB AND PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY: WHAT ARE THE CAUSAL FACTORS? CAN IT BE AVOIDED?

Warnke and colleaguesArticle focus on the scientific rationale for natalizumab in the treatment of multiple sclerosis and the issues related to progressive multifocal leukoencephalopathy causation. Recent results on altered immune surveillance during natalizumab treatment are reviewed. They address the potential effect of our current knowledge on the use of natalizumab in clinical practice.

STATUS EPILEPTICUS OF DIFFERENT CAUSES

Neligan and ShorvonArticle demonstrate in this review that the outcome of status epilepticus is strongly related to the nature of the underlying etiology.

A PHASE 3, DOUBLE-BLIND, PLACEBO-CONTROLLED TRIAL OF IDEBENONE IN FRIEDREICH ATAXIA

Lynch et alArticle report that idebenone did not significantly alter neurological function in Friedreich ataxia during the 6-month study duration.

REPLICATION OF CLU, CR1, AND PICALM ASSOCIATIONS WITH ALZHEIMER DISEASE

Carrasquillo et alArticle have tested for replication of the association between variants in the CLU, CR1, and PICALM genes with Alzheimer disease. Their results, showing near-perfect replication, provide the first additional evidence that CLU, CR1, and PICALM are late-onset Alzheimer disease genes.

PSYCHOSIS IN PARKINSON DISEASE

Forsaa et alArticle provide data that psychotic symptoms affect most patients with Parkinson disease, with increased risk for those with older age at onset, need for high doses of dopaminergic drugs, and with probable rapid eye movement behavior disorder.

ALZHEIMER DISEASE BIOMARKER SIGNATURE

De Meyer and colleaguesArticle sought to identify biomarker patterns typical of Alzheimer disease (AD) in an independent, unsupervised way, without using information on the clinical diagnosis. The mixture modeling approach, totally independent of clinical AD diagnosis, accurately and correctly classified AD patients. The unexpected presence of the AD signature in more than one-third of cognitively normal subjects suggests that AD pathology is active and detectable earlier than has heretofore been envisioned.Article

Place holder to copy figure label and caption

Validation of the combined cerebrospinal fluid–derived β-amyloid protein 1-42 (CSF Aβ1-42)/CSF phosphorylated tau181P (CSF P-Tau181P) mixture model in 2 data sets. A, Patients with mild cognitive impairment who developed Alzheimer disease within 5 years after the CSF sample. B, Patients with autopsy-confirmed Alzheimer disease with mostly less than 1 year between CSF sample and autopsy (n = 68).

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MANAGEMENT OF THROMBOLYSIS-ASSOCIATED SYMPTOMATIC INTRACEREBRAL HEMORRHAGE

Goldstein and colleaguesArticle provide data showing that, in many patients with thrombolysis-associated symptomatic intracerebral hemorrhage after thrombolysis, coagulopathy goes untreated. Continued bleeding after diagnosis in 40% of patients indicates a compelling need for therapeutic intervention.

Α-, Β-, AND Γ-SYNUCLEIN IN DIFFUSE LEWY BODY DISEASE

Nishioka et alArticle report that variants in all 3 members of the synuclein gene family, particularly the α- and γ-synuclein genes SNCA and SNCG, affect the risk of developing diffuse Lewy body disease and warrant further investigation in larger, pathologically defined data sets as well as clinically diagnosed Parkinson disease/dementia with Lewy body case-control series.

AUTONOMIC SYMPTOMS ARE COMMON IN CARRIERS OF THE M.3243 A>G MITOCHONDRIAL DNA MUTATION

Parsons and colleaguesArticle find that m.3243 A>G mutation carriers have frequent autonomic symptoms. The m.3243 A>G mutation should be considered as an etiological factor in patients with autonomic dysfunction and a medical or family history suggestive of mitochondrial disease. They emphasize that some autonomic symptoms are treatable, and so early detection and proactive management may mitigate the burden of morbidity.

THE TRAJECTORY OF GAIT SPEED PRECEDING MILD COGNITIVE IMPAIRMENT

Buracchio et alArticle find that motor decline, as indexed by gait speed, accelerates up to 12 years prior to mild cognitive impairment. Longitudinal changes in motor function may be useful in the early detection of dementia during preclinical stages when the utility of disease-modifying therapies would be greatest.

HEREDITARY CEREBRAL HEMORRHAGE WITH AMYLOIDOSIS ASSOCIATED WITH E693K MUTATION OF APP

Bugiani and colleaguesArticle note that mutations of the β-amyloid precursor protein gene (APP) are linked to familial Alzheimer disease and to autosomal dominant forms of cerebral amyloid angiopathy. Their new findings expand the number of APP mutations linked to hereditary cerebral hemorrhage with amyloidosis, reinforcing the link between this phenotype and codon 693 of APP.

AMYOTROPHIC LATERAL SCLEROSIS–FRONTOTEMPORAL LOBAR DEMENTIA IN 3 FAMILIES WITH P.ALA382THR TARDBP MUTATIONS

Chiò and colleaguesArticle describe 3 apparently unrelated families with familial amyotropic lateral sclerosis (ALS) who carry the p.A382T TARDBP missense mutation and developed frontotemporal lobe dementia (FTLD). In these families, FTLD cosegregates with ALS. Thus, of note, FTLD may develop in patients with ALS who carry TARDBP mutations.

Figures

Place holder to copy figure label and caption

Validation of the combined cerebrospinal fluid–derived β-amyloid protein 1-42 (CSF Aβ1-42)/CSF phosphorylated tau181P (CSF P-Tau181P) mixture model in 2 data sets. A, Patients with mild cognitive impairment who developed Alzheimer disease within 5 years after the CSF sample. B, Patients with autopsy-confirmed Alzheimer disease with mostly less than 1 year between CSF sample and autopsy (n = 68).

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