February 2010 Volume 6 Number 2
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EDITORIAL
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Focus on: Dementia
Dementia: The challenge of dementia therapy
Darran Yates
p57 | doi:10.1038/nrneurol.2009.230
http://links.ealert.nature.com/ctt?kn=62&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
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RESEARCH HIGHLIGHTS
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Focus on: Dementia
Dementia: Biomarker profiles in HIV-associated cognitive disorders and
Alzheimer disease
p59 | doi:10.1038/nrneurol.2009.220
http://links.ealert.nature.com/ctt?kn=59&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
Parkinson disease: Mitochondrial dysfunction occurs early in PD
p60 | doi:10.1038/nrneurol.2009.221
http://links.ealert.nature.com/ctt?kn=61&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
IN BRIEF
Dementia | Epilepsy | Alzheimer disease
p60 | doi:10.1038/nrneurol.2009.226
http://links.ealert.nature.com/ctt?kn=78&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
CORRECTION
New light on an old CLU
p60 | doi:10.1038/nrneurol.2010.13
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Stroke: Indip-a novel neuroprotective agent?
p61 | doi:10.1038/nrneurol.2009.222
http://links.ealert.nature.com/ctt?kn=75&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
Epilepsy: Nonsynaptic mechanisms for interictal discharges in
drug-intractable epilepsy
p61 | doi:10.1038/nrneurol.2009.223
http://links.ealert.nature.com/ctt?kn=74&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
Sleep: Recreational MDMA users at risk of sleep apnea
p62 | doi:10.1038/nrneurol.2009.224
http://links.ealert.nature.com/ctt?kn=73&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
Focus on: Dementia
Dementia: Poor lung function in midlife predicts cognitive decline in men
lacking APOE [epsi]4
p62 | doi:10.1038/nrneurol.2009.225
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NEWS AND VIEWS
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Focus on: Dementia
Dementia: Poststroke dementia-what's in a name?
Anil M. Tuladhar and Frank-Erik de Leeuw
p63 | doi:10.1038/nrneurol.2009.229
Poststroke dementia is a clinically heterogeneous syndrome with various
underlying mechanisms. A better understanding of the pathophysiology of
poststroke dementia together with an improved ability to differentiate
between various dementia syndromes will be useful for optimizing therapeutic
interventions, and for informing patients and carers about treatment options
and prognosis.
http://links.ealert.nature.com/ctt?kn=71&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
Stroke: Delays in the timely diagnosis of stroke in children
Gabrielle A. deVeber
p64 | doi:10.1038/nrneurol.2009.228
Stroke is a frequent cause of neurological morbidity and death in children.
Standardized treatment guidelines for childhood stroke can improve patient
outcomes when such protocols are implemented early after symptom onset.
Medical professionals, however, seem to have a limited awareness of childhood
stroke that perpetuates the delay to diagnosis and, hence, intervention.
http://links.ealert.nature.com/ctt?kn=79&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
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Focus on: Dementia
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REVIEWS
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The clinical use of structural MRI in Alzheimer disease
Giovanni B. Frisoni, Nick C. Fox, Clifford R. Jack Jr, Philip Scheltens
and Paul M. Thompson
p67 | doi:10.1038/nrneurol.2009.215
MRI-based structural imaging has become an integral component of the clinical
assessment of patients with suspected Alzheimer disease (AD), and atrophy
of medial temporal structures is now considered to be a valid diagnostic
marker at the mild cognitive impairment stage. In this article, Frisoni
et al. consider the roles of structural MRI markers in the diagnosis of
AD and non-AD dementias, and in the tracking of disease progression during
clinical trials.
Abstract: http://links.ealert.nature.com/ctt?kn=80&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=81&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
The use of PET in Alzheimer disease
Agneta Nordberg, Juha O. Rinne, Ahmadul Kadir and Bengt Langstrom
p78 | doi:10.1038/nrneurol.2009.217
The underlying pathology in Alzheimer disease is thought to precede the
onset of cognitive symptoms by many years, and efforts are underway to
identify early diagnostic markers and develop disease-modifying treatments
for this condition. Nordberg et al. examine how PET imaging is being used
to further our understanding of the pathophysiology of Alzheimer disease,
and consider future applications of this technique in the clinical setting.
Abstract: http://links.ealert.nature.com/ctt?kn=83&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=93&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
Primary progressive aphasia: clinicopathological correlations
Murray Grossman
p88 | doi:10.1038/nrneurol.2009.216
Primary progressive aphasia (PPA)-a condition characterized by deteriorating
language-is a frequent manifestation of neurodegenerative conditions such
as frontotemporal lobar degeneration. Evidence exists to link the different
PPA variants with specific underlying pathologies and, as Murray Grossman
discusses in this article, knowledge of such clinicopathological correlations
could aid accurate diagnosis of neurodegenerative disease during a patient's
life.
Abstract: http://links.ealert.nature.com/ctt?kn=92&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=96&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
The secretases: enzymes with therapeutic potential in Alzheimer disease
Bart De Strooper, Robert Vassar and Todd Golde
p99 | doi:10.1038/nrneurol.2009.218
The three secretases that process amyloid precursor protein are central
to the generation of amyloid-[beta], and the accumulation of this peptide
in extracellular plaques is one of the hallmarks of Alzheimer disease.
In this Review, De Strooper et al. discuss the evidence that suggests that
these enzymes are potential therapeutic targets for Alzheimer disease drug
treatments.
Abstract: http://links.ealert.nature.com/ctt?kn=94&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=91&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
Can Alzheimer disease be prevented by amyloid-[beta] immunotherapy?
Cynthia A. Lemere and Eliezer Masliah
p108 | doi:10.1038/nrneurol.2009.219
Amyloid-[beta] (A[beta]) has become an important therapeutic target in
Alzheimer disease, and active and passive A[beta] immunotherapies have
been shown to reduce cerebral A[beta] levels and improve cognition in
animal models of this condition. Lemere and Masliah review these preclinical
studies and provide an update on the current status of clinical trials
of A[beta] immunotherapies. They also outline the factors that must be
considered in the future development of such treatments.
Abstract: http://links.ealert.nature.com/ctt?kn=90&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
Article: http://links.ealert.nature.com/ctt?kn=97&m=34611564&r=MTc2NDUyMzIwMwS2&b=2&j=NjcwMjg3NDYS1&mt=1&rt=0
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