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P2‐181: Amino acid sequence of BACE1 and BACE2 determine different subcellular transport and localisation
Author(s) -
Wunderlich Patrick,
Wahle Tina,
Walter Jochen
Publication year - 2008
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2008.05.1255
Subject(s) - adp ribosylation factor , amyloid precursor protein secretase , endosome , amyloid precursor protein , signal transducing adaptor protein , microbiology and biotechnology , golgi apparatus , peptide sequence , biochemistry , plasma protein binding , c terminus , biology , subcellular localization , phosphorylation , chemistry , amino acid , intracellular , alzheimer's disease , cell , gene , medicine , disease , pathology
memory formation--in PrP-MAPT mice that over-express normal human fetal tau (3R/0N isoform). Methods: Field potential recordings were made from the lateral perforant path of the dentate gyrus of either wild-type or heterozygous mice aged 2 and 4 months, respectively, and include assessments of basal transmission, paired-pulse facilitation (PPF) and long-term potentiation (LTP). Results: At 2 months, no difference in the magnitude of LTP between genotypes was observed (Het: 176.4 10.2%, n 6; WT: 171.3 9.1, n 6) but a subtle impairment in basal transmission was detected in the Het’s even at this early age. By 4 months of age, differences in basal transmission, PPF, and LTP (WT: 178.2 6.4, n 6; Het: 148.1 11.9, n 9) were observed. Interestingly, 4M Het LTP data revealed that some slices had normal, WT LTP magnitudes while others were impaired. This duality suggests that at 4 months, Het mice may reside on a threshold between normal and abnormal and that other factors influence the progression of symptoms. Further studies will include assessments in 8-10M old Tau transgenic mice. Conclusions: These data suggest that overexpression of normal tau protein influences hippocampal synaptic properties, similar to deficits found in Tg2576 mice, early in development and thus may be important in the disease progression.