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Neural stem cells genetically-modified to express neprilysin reduce pathology in Alzheimer transgenic models

Bibliographic

Year of Publication:
2014
Contact PI Name:
Mathew Blurton-Jones
Contact PI Affiliation:
Department of Neurobiology and Behavior and Institute for Memory Impairment and Neurological Disorders, University of California Irvine, Irvine, California, USA
Co-Authors:
Brian Spencer, Sara Michael, Nicholas A. Castello, Andranik A. Agazaryan, Joy L. Davis, Franz-Josef Müller, Jeanne F. Loring, Eliezer Masliah, Frank M. LaFerla
Primary Reference (PubMED ID):
Funding Source:
American Health Assistance Foundation
National Institute on Aging (NIA)
Alzheimer's Association
Study Goal and Principal Findings:

Short-term neural stem cell (NSC) transplantation improves cognition in Alzheimer’s disease (AD) transgenic mice by enhancing endogenous synaptic connectivity. However, this approach has no effect on the underlying beta-amyloid (Aβ) and neurofibrillary tangle pathology. Long term efficacy of cell based approaches may therefore require combinatorial approaches. This study genetically-modified NSCs to stably express and secrete the Aβ-degrading enzyme, neprilysin (sNEP). To determine whether sNEP-expressing NSCs can also modulate AD-pathogenesis in vivo, control-modified and sNEP-NSCs were transplanted unilaterally into the hippocampus of two independent and well characterized transgenic models of AD: 3xTg-AD and Thy1-APP mice. After three months, stem cell engraftment, neprilysin expression, and AD pathology were examined. Results reveal that stem cell-mediated delivery of NEP provides marked and significant reductions in Aβ pathology and increases synaptic density in both 3xTg-AD and Thy1-APP transgenic mice. Remarkably, Aβ plaque loads are reduced not only in the hippocampus and subiculum adjacent to engrafted NSCs, but also within the amygdala and medial septum, areas that receive afferent projections from the engrafted region. This data suggest that genetically-modified NSCs could provide a powerful combinatorial approach to not only enhance synaptic plasticity but to also target and modify underlying Alzheimer’s disease pathology.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Biologic - Cell-based
Therapeutic Agent:
sNEP-NSCs (Neprilysin Expressing Neural Stem Cells)
Therapeutic Target:
beta Amyloid Peptide

Animal Model

Model Information:
Species:
Mouse
Model Type:
APPxPS1xTau
Strain/Genetic Background:
C57BL6/129
Species:
Mouse
Model Type:
APP
Strain/Genetic Background:
C57BL/6

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Biomarkers
Dose
Formulation
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest

Outcomes

Outcome Measured
Outcome Parameters
Histopathology
beta Amyloid Load
Neurofibrillary Tau Tangles
Immunochemistry
Activated Microglia
Tau Protein
phospho-Tau
Glial Fibrillary Acidic Protein (GFAP)
Caspase 3
Synaptophysin
Neural Stem Cells
Neprilysin
Activated Microglia
Biochemical
Brain-Derived Neurotrophic Factor (BDNF)
Nestin
Brain-beta Amyloid Peptide 42
Brain-beta Amyloid Peptide 40
Cell Biology
Neurogenesis
Apoptosis
Neuroprotection-Amyloid Neurotoxicity
Cell Viability
Pharmacodynamics
Target Engagement (Reduction beta Amyloid Peptides-Brain)