PMID- 12391602
OWN - NLM
STAT- MEDLINE
DCOM- 20021213
LR  - 20101118
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 70
IP  - 3
DP  - 2002 Nov 1
TI  - Alzheimer's disease: beta-Amyloid protein and tau.
PG  - 392-401
AB  - Research on the molecular pathogenesis of Alzheimer's disease (AD) has made great 
      strides over the last decade. This progress is the result of protein chemical 
      analysis of two extracellular and intracellular fibrillary lesions in AD brain 
      conducted during the 1980s, which identified beta-amyloid protein (A beta) and 
      tau as their major components, respectively. Linkage analysis of familial AD 
      identified four responsible genes: three causative genes (beta-amyloid precursor 
      protein, presenilin 1, and presenilin 2) and one susceptibility gene 
      (apolipoprotein E epsilon 4). All those genes causing and predisposing to AD 
      exhibit a common phenotype: an increased production of A beta 42, a longer, more 
      amyloidogenic A beta species, and/or its enhanced deposition. This observation 
      was substantiated when presenilins were shown to be directly involved in A beta 
      production. Whereas A beta deposition is relatively specific for AD, tau 
      deposition is observed in various neurodegenerative diseases and is assumed to be 
      intimately associated with neuronal loss. The genetic analysis of frontotemporal 
      dementia and parkinsonism linked to chromosome 17 (FTDP-17) revealed the presence 
      of mutations in the tau gene in affected members. Thus, tau can lead to 
      intracellular tau deposits and neuronal loss, although the mechanism remains to 
      be clarified. Taken together, A beta might exert neurotoxicity through tau, 
      leading to neuronal loss in the AD brain.
CI  - Copyright 2002 Wiley-Liss, Inc.
FAU - Morishima-Kawashima, Maho
AU  - Morishima-Kawashima M
AD  - Department of Neuropathology, Faculty of Medicine, University of Tokyo, Tokyo, 
      Japan. maho@m.u-tokyo.ac.jp
FAU - Ihara, Yasuo
AU  - Ihara Y
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Apolipoproteins E)
RN  - 0 (Membrane Proteins)
RN  - 0 (PSEN1 protein, human)
RN  - 0 (Presenilin-1)
RN  - 0 (tau Proteins)
SB  - IM
MH  - Alzheimer Disease/genetics/*metabolism/physiopathology
MH  - Amyloid beta-Peptides/genetics/*metabolism
MH  - Amyloid beta-Protein Precursor/biosynthesis/genetics
MH  - Animals
MH  - Apolipoproteins E/genetics/metabolism
MH  - Cell Death/*physiology
MH  - Chromosomes, Human, Pair 17/genetics
MH  - Humans
MH  - Membrane Proteins/deficiency/genetics
MH  - Mutation/genetics
MH  - Presenilin-1
MH  - tau Proteins/genetics/*metabolism
RF  - 80
EDAT- 2002/10/23 04:00
MHDA- 2002/12/17 04:00
CRDT- 2002/10/23 04:00
PHST- 2002/10/23 04:00 [pubmed]
PHST- 2002/12/17 04:00 [medline]
PHST- 2002/10/23 04:00 [entrez]
AID - 10.1002/jnr.10355 [doi]
PST - ppublish
SO  - J Neurosci Res. 2002 Nov 1;70(3):392-401. doi: 10.1002/jnr.10355.