Literature DB >> 8858181

Presenile because of presenilin: the presenilin genes and early onset Alzheimer's disease.

C Haass1.   

Abstract

Alzheimer's disease is a neurodegenerative disorder characterized by the massive and invariant accumulation of amyloid plaques in the brains of affected patients. In many cases Alzheimer's disease occurs in the absence of a prior history of the disease in other family members and is designated as sporadic, whereas in approximately 10% of patients, dominantly transmitted mutations within one of three genes are found. A few mutations have been identified within the gene encoding the beta-amyloid precursor protein; however, these mutations account for only about 1-3% of cases with familial Alzheimer's disease. In the majority of autosomal dominant cases (40-50%), mutations have been found in a gene localized to chromosome 14. The responsible gene, now called presenilin-1, has recently been identified and shown to encode a putative seven transmembrane domain protein. Surprisingly, a second highly homologous gene (named presenilin-2) was cloned shortly thereafter. It is localized on human chromosome 1 and is also involved in a small number of cases with familial Alzheimer's disease. Early data suggest that mutations found within the two genes cause early onset Alzheimer's disease by influencing the proteolytic processing of amyloid beta-peptide in a pathological manner.

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Year:  1996        PMID: 8858181

Source DB:  PubMed          Journal:  Curr Opin Neurol        ISSN: 1350-7540            Impact factor:   5.710


  6 in total

1.  Notch is required for long-term memory in Drosophila.

Authors:  Asaf Presente; Randy S Boyles; Christine N Serway; J Steven de Belle; Andrew J Andres
Journal:  Proc Natl Acad Sci U S A       Date:  2004-01-29       Impact factor: 11.205

2.  Proteasome inhibitors prevent the degradation of familial Alzheimer's disease-linked presenilin 1 and potentiate A beta 42 recovery from human cells.

Authors:  P Marambaud; K Ancolio; E Lopez-Perez; F Checler
Journal:  Mol Med       Date:  1998-03       Impact factor: 6.354

3.  Proteolytic processing of the Alzheimer disease-associated presenilin-1 generates an in vivo substrate for protein kinase C.

Authors:  J Walter; J Grünberg; A Capell; B Pesold; A Schindzielorz; M Citron; K Mendla; P S George-Hyslop; G Multhaup; D J Selkoe; C Haass
Journal:  Proc Natl Acad Sci U S A       Date:  1997-05-13       Impact factor: 11.205

4.  The Alzheimer's disease-associated presenilins are differentially phosphorylated proteins located predominantly within the endoplasmic reticulum.

Authors:  J Walter; A Capell; J Grünberg; B Pesold; A Schindzielorz; R Prior; M B Podlisny; P Fraser; P S Hyslop; D J Selkoe; C Haass
Journal:  Mol Med       Date:  1996-11       Impact factor: 6.354

Review 5.  Mechanisms of islet amyloidosis toxicity in type 2 diabetes.

Authors:  Andisheh Abedini; Ann Marie Schmidt
Journal:  FEBS Lett       Date:  2013-01-18       Impact factor: 4.124

6.  Cortical neurons transgenic for human Abeta40 or Abeta42 have similar vulnerability to apoptosis despite their different amyloidogenic properties.

Authors:  Najeeb A Shiwany; Jun Xie; Qing Guo
Journal:  Int J Clin Exp Pathol       Date:  2008-11-26
  6 in total

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