Linked Life Data

17168641

Source:http://linkedlifedata.com/resource/pubmed/id/17168641

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2006-12-15
pubmed:abstractText
Advances in the understanding of Alzheimer's disease (AD) pathogenesis provide strong support for a modified version of the amyloid cascade hypothesis, which is now often referred to as the amyloid beta protein (Abeta) cascade hypothesis. The basic tenant of this modified hypothesis is that Abeta aggregates trigger a complex pathological cascade leading to neurodegeneration. Thus, as opposed to the original amyloid hypothesis, whose basic tenant was that amyloid deposits cause AD, the Abeta hypothesis is more inclusive in that it takes into account the possibility that several different Abeta assemblies might contribute to AD pathogenesis and not merely the detectable amyloid deposits within the brain. Significantly, the Abeta hypothesis has provided the rationale for a plethora of therapeutic interventions that target Abeta production, aggregation or clearance. Indeed, AD research is entering an exciting phase in which strategies derived from basic research will be tested in humans. Despite this progress, many aspects of AD pathogenesis, particularly those downstream of Abeta accumulation are not well understood. Herein, we explore several observations that serve to illustrate the more enigmatic aspects of the Abeta hypothesis, and discuss why further basic research may be critical in order to develop therapies designed to halt neurodegeneration and reverse cognitive decline in patients already suffering from AD dementia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1567-2050
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
421-30
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Filling the gaps in the abeta cascade hypothesis of Alzheimer's disease.
pubmed:affiliation
Mayo Clinic College of Medicine, Department of Neuroscience, Mayo Clinic Jacksonville 4500 San Pablo Rd., Jacksonville, Florida 32224, USA. tgolde@mayo.edu
pubmed:publicationType
Journal Article, Review