With human life spans continuing to increase worldwide, the ability to keep brain functions intact into old age becomes ever more important. As the articles in this Clinical Collection illustrate, approaches to preventing or arresting neurodegeneration can take many forms, from lifestyle changes aimed at preserving the integrity of the brain, to pharmacological treatments and immunological interventions targeted at specific neurodegenerative disease mechanisms.
Produced with support of a grant from Teva Pharmaceuticals
NEWS & VIEWS
Alzheimer disease: Insulin resistance and AD—extending the translational path
Suzanne Craft
doi:10.1038/nrneurol.2012.112
Nature Reviews Neurology 8, 360-362 (2012)
Movement disorders in 2012: Advancing research towards novel therapeutic approaches
Nikolaus R. McFarland & Michael S. Okun
doi:10.1038/nrneurol.2012.265
Nature Reviews Neurology 9, 70-71 (2013)
REVIEWS
Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy
Chia-Chen Liu, Takahisa Kanekiyo, Huaxi Xu & Guojun Bu
doi:10.1038/nrneurol.2012.263
Nature Reviews Neurology 9, 106-118 (2013)
The ε4 allele of the apolipoprotein E (APOE) gene is the strongest genetic risk factor for Alzheimer disease (AD). Guojun Bu and colleagues describe the pathogenic links between Apo-E4 and neurodegeneration, including amyloid-β-dependent mechanisms and impairment of neurovascular function. The authors suggest potential strategies to target Apo-E, which could provide important additions to therapeutic options for AD.
Control of autophagy as a therapy for neurodegenerative disease
Harry Harris & David C. Rubinsztein
doi:10.1038/nrneurol.2011.200
Nature Reviews Neurology 8, 108-117 (2012)
Defects in autophagy—a process that enables the degradation of unwanted or damaged intracellular proteins and organelles—are associated with the accumulation of aggregate-prone proteins. Defects in neuronal autophagy may have a role in neurodegenerative disease that are associated with aberrant protein accumulation, such as Alzheimer disease and Parkinson disease. Rubinsztein and Harris discuss how defects in autophagic pathways might cause these diseases and highlight how autophagy-modulating drugs might be used as therapy.
Modifiable factors that alter the size of the hippocampus with ageing
Majid Fotuhi, David Do & Clifford Jack
doi:10.1038/nrneurol.2012.27
Nature Reviews Neurology 8, 189-202 (2012)
The hippocampus is a dynamic structure that can change in size throughout life. Hippocampal atrophy, which is associated with cognitive decline and late-life dementia, can be exacerbated by a number of medical conditions. In this Review, Fotuhi and colleagues examine the modifiable factors that can affect hippocampal size, and discuss lifestyle and therapeutic interventions that might prevent or even reverse hippocampal atrophy.
PERSPECTIVES
Preclinical Alzheimer disease—the challenges ahead
Reisa A. Sperling, Jason Karlawish & Keith A. Johnson
doi:10.1038/nrneurol.2012.241
Nature Reviews Neurology 9, 54-58 (2013)
Pathological changes underlying Alzheimer disease (AD) begin more than 10 years before clinical presentation, and the need for early therapeutic intervention is becoming increasingly recognized. Reisa Sperling and colleagues consider challenges to such an approach—including the difficulty of defining preclinical AD, and ethical issues associated with disclosing information on AD biomarker status to healthy individuals—and discuss possible ways to overcome these hurdles.
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