PMID- 29376876
OWN - NLM
STAT- MEDLINE
DCOM- 20190124
LR  - 20190124
IS  - 1875-8908 (Electronic)
IS  - 1387-2877 (Linking)
VI  - 61
IP  - 4
DP  - 2018
TI  - Endogenous Murine Amyloid-beta Peptide Assembles into Aggregates in the Aged 
      C57BL/6J Mouse Suggesting These Animals as a Model to Study Pathogenesis of 
      Amyloid-beta Plaque Formation.
PG  - 1425-1450
LID - 10.3233/JAD-170923 [doi]
AB  - Amyloid-beta peptide (Abeta), paired helical filament-tau (PHF-tau), and alpha-synuclein 
      are in the focus of neuroscience research because they aggregate in brains of 
      patients with Alzheimer's and Parkinson's diseases. For this purpose, transgenic 
      mouse models were used containing the human genes for AbetaPP/presenilin/tau or 
      alpha-synuclein with the most frequent mutations. This is not ideal because most 
      patients develop sporadic forms of the diseases with no causative single gene 
      defect and furthermore the aggregation of human proteins in man is not 
      necessarily the same in rodents. We hypothesized that for such cases the aged 
      mouse could be an alternative model and analyzed the distribution of endogenous 
      Abeta, PHF-tau, and alpha-synuclein in mouse brains at different ages. Whereas Abeta was 
      below detectable levels at birth, it was present at high levels in the 
      15-month-old mouse. Abeta was found in the cytosol and lysosomes of neurons of the 
      temporal cortex, cingulate area, pons, and cerebellum as well as extracellularly 
      in the periventricular zone. Contrary to Abeta, mouse brain was devoid of 
      PHF-tau-positive neurofibrillary tangles. alpha-Synuclein was detectable in the 
      newborn mouse with highest levels in the marginal zone of the lateral cortex and 
      average levels in the hippocampus, pons, and cerebellum. Brain-area specific 
      differences in the alpha-synuclein level persisted up to 15 months of age, but 
      increased 3-fold in all areas over time. alpha-Synuclein resided in the neuropil, but 
      not in intracellular aggregates even in the aged mouse. We suggest the aged mouse 
      as a model to study Abeta plaque formation.
FAU - Ahlemeyer, Barbara
AU  - Ahlemeyer B
AD  - Institute for Anatomy and Cell Biology, Division of Medical Cell Biology, Justus 
      Liebig University, Giessen, Germany.
FAU - Halupczok, Sascha
AU  - Halupczok S
AD  - Institute for Anatomy and Cell Biology, Division of Medical Cell Biology, Justus 
      Liebig University, Giessen, Germany.
FAU - Rodenberg-Frank, Elke
AU  - Rodenberg-Frank E
AD  - Institute for Anatomy and Cell Biology, Division of Medical Cell Biology, Justus 
      Liebig University, Giessen, Germany.
FAU - Valerius, Klaus-Peter
AU  - Valerius KP
AD  - Institute for Anatomy and Cell Biology, Division of Medical Cell Biology, Justus 
      Liebig University, Giessen, Germany.
FAU - Baumgart-Vogt, Eveline
AU  - Baumgart-Vogt E
AD  - Institute for Anatomy and Cell Biology, Division of Medical Cell Biology, Justus 
      Liebig University, Giessen, Germany.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - J Alzheimers Dis
JT  - Journal of Alzheimer's disease : JAD
JID - 9814863
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (alpha-Synuclein)
RN  - 0 (tau Proteins)
SB  - IM
MH  - Age Factors
MH  - Aged
MH  - Aged, 80 and over
MH  - Alzheimer Disease/*genetics/pathology
MH  - Amyloid beta-Peptides/metabolism
MH  - Animals
MH  - Brain/*pathology
MH  - *Disease Models, Animal
MH  - Female
MH  - Humans
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Neurofibrillary Tangles/pathology
MH  - Neurons/metabolism
MH  - Plaque, Amyloid/pathology
MH  - alpha-Synuclein/*metabolism
MH  - tau Proteins/*metabolism
OTO - NOTNLM
OT  - Aged mouse
OT  - PHF-tau
OT  - amyloid-beta peptides
OT  - brain regions
OT  - extracellular aggregates
OT  - alpha-synuclein
EDAT- 2018/01/30 06:00
MHDA- 2019/01/25 06:00
CRDT- 2018/01/30 06:00
PHST- 2018/01/30 06:00 [entrez]
PHST- 2018/01/30 06:00 [pubmed]
PHST- 2019/01/25 06:00 [medline]
AID - JAD170923 [pii]
AID - 10.3233/JAD-170923 [doi]
PST - ppublish
SO  - J Alzheimers Dis. 2018;61(4):1425-1450. doi: 10.3233/JAD-170923.