Alzheimer's disease.

Abstract

Alzheimer's disease (AD) is the most commonly diagnosed etiology of dementia and may be caused by the progressive accumulation and deposition of neurotoxic Abeta/amyloid plaques and aggregates in brain with aging-the amyloid hypothesis of AD. However, Abeta/amyloid deposition is likely necessary but not sufficient to cause AD, and other putative downstream pathologies, including the aggregation of phospho-tau in neurofibrillary tangles, synaptic and neuronal loss, and glial and inflammatory responses, are likely equally important to AD pathogenesis. The majority of AD is sporadic (> 95%) but the discovery of rare early onset familial forms of AD has been pivotal to our understanding of its pathogenesis and in developing novel therapeutic strategies. Currently available drugs for patients with AD provide modest, temporary, and palliative benefits, but they consistently demonstrate safety and efficacy on cognitive, functional, behavioral, and global outcome measures. Novel potential disease-modifying therapies now in preclinical research or clinical trials may be more effective in preventing or arresting the progressive dementia of AD and will provide a test of the amyloid hypothesis.

• Authors: R Scott Turner
• Journal: Seminars in neurology (Semin Neurol) Vol. 26 Issue 5 Pg. 499-506 (Nov 2006) ISSN: 0271-8235 [Print] United States
• PMID: 17048151 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)

Chemical References

• Amyloid beta-Peptides

Topics

• Alzheimer Disease (genetics, pathology, physiopathology)
• Amyloid beta-Peptides
• Animals
• Mice
• Neurofibrillary Tangles
• Risk Factors