PMID- 15615650
OWN - NLM
STAT- MEDLINE
DCOM- 20050203
LR  - 20161126
IS  - 0006-3002 (Print)
IS  - 0006-3002 (Linking)
VI  - 1739
IP  - 2-3
DP  - 2005 Jan 3
TI  - Tau alteration and neuronal degeneration in tauopathies: mechanisms and models.
PG  - 331-54
AB  - Tau becomes characteristically altered both functionally and structurally in 
      several neurodegenerative diseases now collectively called tauopathies. Although 
      increasing evidence supports that alterations of tau may directly cause neuronal 
      degeneration and cell death, the mechanisms, which render tau to become a toxic 
      agent are still unclear. In addition, it is obscure, whether neurodegeneration in 
      tauopathies occurs via a common mechanism or specific differences exist. The aim 
      of this review is to provide an overview about the different experimental models 
      that currently exist, how they are used to determine the role of tau during 
      degeneration and what has been learnt from them concerning the mechanistic role 
      of tau in the disease process. The review begins with a discussion about 
      similarities and differences in tau alteration in paradigmatic tauopathies such 
      as frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) and 
      Alzheimer's disease (AD). The second part concentrates on major experimental 
      models that have been used to address the mechanistic role of tau during 
      degeneration. This will include a discussion of cell-free assays, culture models 
      using cell lines or dissociated neurons, and animal models. How these models aid 
      to understand (i) alterations in the function of tau as a microtubule-associated 
      protein (MAP), (ii) direct cytotoxicity of altered tau protein, and (iii) the 
      potential role of tau aggregation in neurodegenerative processes will be the 
      central theme of this part. The review ends with concluding remarks about a 
      general mechanistic model of the role of tau alteration and neuronal degeneration 
      in tauopathies and future perspectives.
FAU - Brandt, Roland
AU  - Brandt R
AD  - Department of Neurobiology, University of Osnabruck, Barbarastrasse 11, D-49076 
      Osnabruck, Germany. Brandt@biologie.uni-osnabrueck.de
FAU - Hundelt, Monika
AU  - Hundelt M
FAU - Shahani, Neelam
AU  - Shahani N
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Netherlands
TA  - Biochim Biophys Acta
JT  - Biochimica et biophysica acta
JID - 0217513
RN  - 0 (Protein Isoforms)
RN  - 0 (tau Proteins)
SB  - IM
MH  - Alzheimer Disease/metabolism/pathology
MH  - Animals
MH  - Cells, Cultured
MH  - Chromosomes, Human, Pair 17
MH  - Dementia/metabolism
MH  - Humans
MH  - Mice
MH  - Mice, Transgenic
MH  - Models, Biological
MH  - Mutation
MH  - Nerve Degeneration/metabolism
MH  - Neurofibrillary Tangles
MH  - Parkinson Disease/metabolism
MH  - Protein Isoforms/metabolism
MH  - Tauopathies/*metabolism
MH  - tau Proteins/genetics/*metabolism/physiology
RF  - 228
EDAT- 2004/12/24 09:00
MHDA- 2005/02/04 09:00
CRDT- 2004/12/24 09:00
PHST- 2004/05/05 00:00 [received]
PHST- 2004/06/15 00:00 [accepted]
PHST- 2004/12/24 09:00 [pubmed]
PHST- 2005/02/04 09:00 [medline]
PHST- 2004/12/24 09:00 [entrez]
AID - S0925-4439(04)00110-3 [pii]
AID - 10.1016/j.bbadis.2004.06.018 [doi]
PST - ppublish
SO  - Biochim Biophys Acta. 2005 Jan 3;1739(2-3):331-54. doi: 
      10.1016/j.bbadis.2004.06.018.