Twenty years of the Alzheimer's disease amyloid hypothesis: a genetic perspective

Rudolph E Tanzi; Lars Bertram

doi:10.1016/j.cell.2005.02.008

Twenty years of the Alzheimer's disease amyloid hypothesis: a genetic perspective

Cell. 2005 Feb 25;120(4):545-55. doi: 10.1016/j.cell.2005.02.008.

Authors

Rudolph E Tanzi¹, Lars Bertram

Affiliation

¹ Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Diseases, Department of Neurology, Massachussetts General Hospital, Harvard Medical School, Charlestown, Massachussetts 02129, USA. tanzi@helix.mgh.harvard.edu

PMID: 15734686
DOI: 10.1016/j.cell.2005.02.008

Abstract

From Alois Alzheimer's description of Auguste D.'s brain in 1907 to George Glenner's biochemical dissection of beta-amyloid in 1984, the "amyloid hypothesis" of Alzheimer's disease has continued to gain support over the past two decades, particularly from genetic studies. Here we assess the amyloid hypothesis based on both known and putative Alzheimer's disease genes.

Publication types

Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

MeSH terms

Alzheimer Disease* / etiology
Alzheimer Disease* / genetics
Alzheimer Disease* / metabolism
Alzheimer Disease* / physiopathology
Amyloid Precursor Protein Secretases
Amyloid beta-Peptides / genetics*
Amyloid beta-Peptides / metabolism
Amyloid beta-Protein Precursor / genetics*
Amyloid beta-Protein Precursor / metabolism
Aspartic Acid Endopeptidases
Chromosomes, Human, Pair 21 / genetics*
Chromosomes, Human, Pair 21 / metabolism
Endopeptidases / genetics
Endopeptidases / metabolism
Humans
Mutation / genetics
Protein Denaturation / genetics
Protein Denaturation / physiology

Substances

Amyloid beta-Peptides
Amyloid beta-Protein Precursor
Amyloid Precursor Protein Secretases
Endopeptidases
Aspartic Acid Endopeptidases
BACE1 protein, human