With the growth of the aged population, the socioeconomic costs of dementia are set to rise sharply. No disease-modifying drugs currently exist for the main cause of dementia, namely Alzheimer disease. The successful development of such drugs, and disease-modifying therapies for other causes of dementia, will require the ability to make an early diagnosis of the disease and a means to monitor the progression of pathology in vivo, in addition to novel agents. In this Focus issue, leading experts examine pharmacological strategies that are being explored to combat Alzheimer disease and biomarkers that are being developed for this disorder and other causes of dementia.
EDITORIAL
Dementia: The challenge of dementia therapy
Darran Yates
doi:10.1038/nrneurol.2009.230
Nature Reviews Neurology 6, 57 (2010)
RESEARCH HIGHLIGHTS
Dementia: Biomarker profiles in HIV-associated cognitive disorders and Alzheimer disease
Darran Yates
doi:10.1038/nrneurol.2009.220
Nature Reviews Neurology 6, 59 (2010)
Dementia: Poor lung function in midlife predicts cognitive decline in men lacking APOE ϵ4
Rowan Higgs
doi:10.1038/nrneurol.2009.225
Nature Reviews Neurology 6, 70 (2010)
NEWS AND VIEWS
Dementia: Poststroke dementia—what's in a name?
Anil M. Tuladhar & Frank-Erik de Leeuw
doi:10.1038/nrneurol.2009.229
Nature Reviews Neurology 6, 63-64 (2010)
REVIEWS
The clinical use of structural MRI in Alzheimer disease
Giovanni B. Frisoni, Nick C. Fox, Clifford R. Jack, Jr, Philip Scheltens & Paul M. Thompson
doi:10.1038/nrneurol.2009.215
Nature Reviews Neurology 6, 67-77 (2010)
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.
The use of PET in Alzheimer disease
Agneta Nordberg, Juha O. Rinne, Ahmadul Kadir & Bengt Långström
doi:10.1038/nrneurol.2009.217
Nature Reviews Neurology 6, 78-87 (2010)
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.
Primary progressive aphasia: clinicopathological correlations
Murray Grossman
doi:10.1038/nrneurol.2009.216
Nature Reviews Neurology 6, 88-97 (2010)
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.
The secretases: enzymes with therapeutic potential in Alzheimer disease
Bart De Strooper, Robert Vassar & Todd Golde
doi:10.1038/nrneurol.2009.218
Nature Reviews Neurology 6, 99-107 (2010)
The three secretases that process amyloid precursor protein are central to the generation of amyloid-β, 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.
Can Alzheimer disease be prevented by amyloid-β immunotherapy?
Cynthia A. Lemere & Eliezer Masliah
doi:10.1038/nrneurol.2009.219
Nature Reviews Neurology 6, 108-119 (2010)
Amyloid-β (Aβ) has become an important therapeutic target in Alzheimer disease, and active and passive Aβ immunotherapies have been shown to reduce cerebral Aβ 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 Aβ immunotherapies. They also outline the factors that must be considered in the future development of such treatments.
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