Alzheimer's disease.

Saved in:
Bibliographic Details
Title: Alzheimer's disease.
Authors: Blennow K (AUTHOR), de Leon MJ (AUTHOR), Zetterberg H (AUTHOR), Blennow, Kaj (AUTHOR), de Leon, Mony J (AUTHOR), Zetterberg, Henrik (AUTHOR)
Source: Lancet. 7/29/2006, Vol. 368 Issue 9533, p387-403. 17p.
Abstract: Alzheimer's disease is the most common cause of dementia. Research advances have enabled detailed understanding of the molecular pathogenesis of the hallmarks of the disease--ie, plaques, composed of amyloid beta (Abeta), and tangles, composed of hyperphosphorylated tau. However, as our knowledge increases so does our appreciation for the pathogenic complexity of the disorder. Familial Alzheimer's disease is a very rare autosomal dominant disease with early onset, caused by mutations in the amyloid precursor protein and presenilin genes, both linked to Abeta metabolism. By contrast with familial disease, sporadic Alzheimer's disease is very common with more than 15 million people affected worldwide. The cause of the sporadic form of the disease is unknown, probably because the disease is heterogeneous, caused by ageing in concert with a complex interaction of both genetic and environmental risk factors. This seminar reviews the key aspects of the disease, including epidemiology, genetics, pathogenesis, diagnosis, and treatment, as well as recent developments and controversies. [ABSTRACT FROM AUTHOR]
Copyright of Lancet is the property of Lancet and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
FullText Links:
  – Type: pdflink
Text:
  Availability: 0
Header DbId: pbh
DbLabel: Psychology and Behavioral Sciences Collection
An: 106003161
AccessLevel: 6
PubType: Academic Journal
PubTypeId: academicJournal
PreciseRelevancyScore: 0
IllustrationInfo
Items – Name: Title
  Label: Title
  Group: Ti
  Data: Alzheimer's disease.
– Name: Author
  Label: Authors
  Group: Au
  Data: <searchLink fieldCode="AR" term="%22Blennow+K%22">Blennow K</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22de+Leon+MJ%22">de Leon MJ</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zetterberg+H%22">Zetterberg H</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Blennow%2C+Kaj%22">Blennow, Kaj</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22de+Leon%2C+Mony+J%22">de Leon, Mony J</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zetterberg%2C+Henrik%22">Zetterberg, Henrik</searchLink> (AUTHOR)
– Name: TitleSource
  Label: Source
  Group: Src
  Data: <searchLink fieldCode="JN" term="%22Lancet%22">Lancet</searchLink>. 7/29/2006, Vol. 368 Issue 9533, p387-403. 17p.
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Alzheimer's disease is the most common cause of dementia. Research advances have enabled detailed understanding of the molecular pathogenesis of the hallmarks of the disease--ie, plaques, composed of amyloid beta (Abeta), and tangles, composed of hyperphosphorylated tau. However, as our knowledge increases so does our appreciation for the pathogenic complexity of the disorder. Familial Alzheimer's disease is a very rare autosomal dominant disease with early onset, caused by mutations in the amyloid precursor protein and presenilin genes, both linked to Abeta metabolism. By contrast with familial disease, sporadic Alzheimer's disease is very common with more than 15 million people affected worldwide. The cause of the sporadic form of the disease is unknown, probably because the disease is heterogeneous, caused by ageing in concert with a complex interaction of both genetic and environmental risk factors. This seminar reviews the key aspects of the disease, including epidemiology, genetics, pathogenesis, diagnosis, and treatment, as well as recent developments and controversies. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Lancet is the property of Lancet and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
PLink https://search.ebscohost.com/login.aspx?direct=true&site=eds-live&db=pbh&AN=106003161
RecordInfo BibRecord:
  BibEntity:
    Identifiers:
      – Type: doi
        Value: 10.1016/s0140-6736(06)69113-7
    Languages:
      – Code: eng
        Text: English
    PhysicalDescription:
      Pagination:
        PageCount: 17
        StartPage: 387
    Titles:
      – TitleFull: Alzheimer's disease.
        Type: main
  BibRelationships:
    HasContributorRelationships:
      – PersonEntity:
          Name:
            NameFull: Blennow K
      – PersonEntity:
          Name:
            NameFull: de Leon MJ
      – PersonEntity:
          Name:
            NameFull: Zetterberg H
      – PersonEntity:
          Name:
            NameFull: Blennow, Kaj
      – PersonEntity:
          Name:
            NameFull: de Leon, Mony J
      – PersonEntity:
          Name:
            NameFull: Zetterberg, Henrik
    IsPartOfRelationships:
      – BibEntity:
          Dates:
            – D: 29
              M: 07
              Text: 7/29/2006
              Type: published
              Y: 2006
          Identifiers:
            – Type: issn-print
              Value: 01406736
          Numbering:
            – Type: volume
              Value: 368
            – Type: issue
              Value: 9533
          Titles:
            – TitleFull: Lancet
              Type: main
ResultId 1