Plasma amyloid β‐peptide 1–42 and incipient Alzheimer's disease

Mutations in the amyloid precursor protein and presenilin 1 and 2 genes result in elevated plasma levels of the amyloid β‐peptide species terminating at amino acid residue 42 (Aβ1–42). In a longitudinal study of unrelated elderly individuals, those who subsequently developed Alzheimer's disease had higher plasma levels of Aβ1–42 at entry than did those who remained free of dementia. The results indicate that elevated plasma levels of the released Aβ peptide Aβ1–42 may be detected several years before the onset of symptoms, supporting that extracellular Aβ1–42 plays an important role in the pathogenesis of late‐onset Alzheimer's disease.

[1]  B Engvall,et al.  Cerebrospinal fluid Aβ42 is increased early in sporadic Alzheimer's disease and declines with disease progression , 1999, Annals of neurology.

[2]  P. Mehta,et al.  Quantification of sub-femtomole amounts of Alzheimer amyloid β peptides , 1999 .

[3]  H. Wiśniewski,et al.  Increased plasma amyloid β protein 1–42 levels in Down syndrome , 1998, Neuroscience Letters.

[4]  S. Paul,et al.  Lack of apolipoprotein E dramatically reduces amyloid β-peptide deposition , 1997, Nature Genetics.

[5]  D. Selkoe,et al.  Enhanced Production and Oligomerization of the 42-residue Amyloid β-Protein by Chinese Hamster Ovary Cells Stably Expressing Mutant Presenilins* , 1997, The Journal of Biological Chemistry.

[6]  S. Tsuji,et al.  The beta APP717 Alzheimer mutation increases the percentage of plasma amyloid-beta protein ending at A beta 42(43) , 1997, Neurology.

[7]  Weiming Xia,et al.  Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice , 1997, Nature Medicine.

[8]  Allan I. Levey,et al.  Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo , 1996, Neuron.

[9]  J. Hardy,et al.  Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1 , 1996, Nature.

[10]  G. Schellenberg,et al.  Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease , 1996, Nature Medicine.

[11]  R. Wolfert,et al.  Reduction of β‐amyloid peptide42 in the cerebrospinal fluid of patients with Alzheimer's disease , 1995 .

[12]  D. Mann,et al.  Amyloid β protein (Aβ) deposition: Aβ42(43) precedes Aβ40 in down Syndrome , 1995, Annals of neurology.

[13]  T. Iwatsubo,et al.  Visualization of Aβ42(43) and Aβ40 in senile plaques with end-specific Aβ monoclonals: Evidence that an initially deposited species is Aβ42(43) , 1994, Neuron.

[14]  R. Mayeux,et al.  Diagnosis of dementia in a heterogeneous population. Development of a neuropsychological paradigm-based diagnosis of dementia and quantified correction for the effects of education. , 1992, Archives of neurology.

[15]  M. Folstein,et al.  Clinical diagnosis of Alzheimer's disease , 1984, Neurology.

[16]  C. P. Hughes,et al.  A New Clinical Scale for the Staging of Dementia , 1982, British Journal of Psychiatry.