Mice Overexpressing Amyloid Precursor Protein and Tau in the Cerebrospinal Fluid of Transgenic β Changes in Amyloid -

for understanding events in human disease. and Tau in the CSF of AD patients. They also suggest the translational value of APP mouse models β changes in A deposition in the brain may be the driving force for β became prominent. Mechanistically, these results suggest that A deposition started and that CSF t-Tau increased when amyloid plaques in mouse brain β mouse CSF decreased as A 42 concentration in β pathology. They found that the A β models, with different ages of onset and progression of A peptides and total Tau in the CSF of two different APP transgenic mouse β then used these assays to measure A peptides and total Tau in mouse CSF. They β collecting mouse CSF and validated sensitive assays for detecting A optimized methods for et al. pathology, but CSF markers have not been investigated. To this end, Maia β model A of early, preclinical AD. Transgenic mice overexpressing human amyloid precursor protein (APP) have been used to (CSF) amyloid plaques and neurofibrillary tangles, respectively, have shown promise as markers in cerebrospinal fluid ) peptide and Tau protein, the constituents of the pathological hallmarks of AD, β (A β clinical symptoms. Amyloideffective when given at a preclinical stage of disease before neurodegeneration has become severe enough to induce symptoms in both sporadic and familial forms of the disease. Thus, disease-modifying drugs will most likely be The pathology of Alzheimer's disease (AD) is thought to start 10 to 20 years before the onset of the first clinical From Bedside Back to Bench