Abstract
Apathy is an early and common neuropsychiatric syndrome in Alzheimer’s disease (AD) patients. In clinical trials, apathy is associated with decreased motor activity that can be monitored by actigraphy. The triple transgenic mouse AD model (3xTgAD) has been shown to recapitulate the biochemical lesions as well as many of the synaptic and cognitive alterations associated with AD. In the present work we found that these mice also develop an early and consistent apathy-like behavior as evidenced by a drastic decrease in spontaneous activity measured by actimetry. We recently established that these mice also display an intraneuronal accumulation of the β-secretase-derived βAPP fragment (C99) appearing early, in absence of Aβ. Interestingly, we found that the apathy-like behavior observed in 3xTgAD mice was temporally associated with C99 accumulation and synaptic alterations. Since it is well known that the genetic background can strongly influence behavior and can induce transcriptional variability in animal models, we decided to determine the influence of genetic background on the above-described alterations. We backcrossed 3xTgAD mice to C57BL/6 and found that the genetic background had no influence on either C99 accumulation or synaptic plasticity alterations, but strongly affected the apathy-like behavior.
Keywords: Apathy, behavior, C99, LTP, immunohistochemistry, triple transgenic mice, genetic background.
Current Alzheimer Research
Title:Influence of Genetic Background on Apathy-Like Behavior in Triple Transgenic AD Mice
Volume: 13 Issue: 8
Author(s): R. Pardossi-Piquard, I. Lauritzen, C. Bauer, G. Sacco, P. Robert and F. Checler
Affiliation:
Keywords: Apathy, behavior, C99, LTP, immunohistochemistry, triple transgenic mice, genetic background.
Abstract: Apathy is an early and common neuropsychiatric syndrome in Alzheimer’s disease (AD) patients. In clinical trials, apathy is associated with decreased motor activity that can be monitored by actigraphy. The triple transgenic mouse AD model (3xTgAD) has been shown to recapitulate the biochemical lesions as well as many of the synaptic and cognitive alterations associated with AD. In the present work we found that these mice also develop an early and consistent apathy-like behavior as evidenced by a drastic decrease in spontaneous activity measured by actimetry. We recently established that these mice also display an intraneuronal accumulation of the β-secretase-derived βAPP fragment (C99) appearing early, in absence of Aβ. Interestingly, we found that the apathy-like behavior observed in 3xTgAD mice was temporally associated with C99 accumulation and synaptic alterations. Since it is well known that the genetic background can strongly influence behavior and can induce transcriptional variability in animal models, we decided to determine the influence of genetic background on the above-described alterations. We backcrossed 3xTgAD mice to C57BL/6 and found that the genetic background had no influence on either C99 accumulation or synaptic plasticity alterations, but strongly affected the apathy-like behavior.
Export Options
About this article
Cite this article as:
Pardossi-Piquard R., Lauritzen I., Bauer C., Sacco G., Robert P. and Checler F., Influence of Genetic Background on Apathy-Like Behavior in Triple Transgenic AD Mice, Current Alzheimer Research 2016; 13 (8) . https://dx.doi.org/10.2174/1567205013666160404120106
DOI https://dx.doi.org/10.2174/1567205013666160404120106 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
Call for Papers in Thematic Issues
New Advances in the Prevention, Diagnosis, Treatment, and Rehabilitation of Alzheimer's Disease
Aims and Scope: Introduction: Alzheimer's disease (AD) poses a significant global health challenge, with an increasing prevalence that demands concerted efforts to advance our understanding and strategies for prevention, diagnosis, treatment, and rehabilitation. This thematic issue aims to bring together cutting-edge research and innovative approaches from multidisciplinary perspectives to address ...read more
Current updates on the Role of Neuroinflammation in Neurodegenerative Disorders
Neuroinflammation is an invariable hallmark of chronic and acute neurodegenerative disorders and has long been considered a potential drug target for Alzheimer?s disease (AD) and dementia. Significant evidence of inflammatory processes as a feature of AD is provided by the presence of inflammatory markers in plasma, CSF and postmortem brain ...read more
Deep Learning for Advancing Alzheimer's Disease Research
Alzheimer's disease (AD) poses a significant global health challenge, with an increasing number of individuals affected yearly. Deep learning, a subfield of artificial intelligence, has shown immense potential in various domains, including healthcare. This thematic issue of Current Alzheimer Research explores the application of deep learning techniques in advancing our ...read more
Diagnostic and therapeutic biomarkers of dementia
Dementia affects 18 million people worldwide. Dementia is a syndrome of symptoms caused by brain disease, usually chronic or progressive, clinically characterized by multiple impairments of higher cortical functions such as memory, thinking, orientation, and learning. In addition, in the course of dementia, cognitive deficits are observed, which often hinder ...read more
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Effects of Resveratrol and Other Polyphenols on the Most Common Brain Age-Related Diseases
Current Medicinal Chemistry Pro-Inflammatory Cytokines IL-1β and TNF-α are not Associated with Plasma Homocysteine Concentration in Alzheimer’s Disease
Current Alzheimer Research Secondary Stroke Prevention in Patients with Cryptogenic Stroke and Patent Foramen Ovale
Vascular Disease Prevention (Discontinued) Targeting Inhibition of COX-2: A Review of Patents, 2002 - 2006
Recent Patents on Inflammation & Allergy Drug Discovery A Comprehensive Investigation of Molecular Signatures and Pathways Linking Alzheimer’s Disease and Epilepsy <i>via</i> Bioinformatic Approaches
Current Alzheimer Research Antioxidant Properties of Melatonin and its Potential Action in Diseases
Current Topics in Medicinal Chemistry Statins: Are They All the Same?
Current Drug Therapy Psoriasis and Atherosclerosis: Is There a Need For Novel Biomarkers Assessing Cardiovascular Risk?
Current Pharmaceutical Design Pyroglutamate-Modified Amyloid Beta Peptides: Emerging Targets for Alzheimer´s Disease Immunotherapy
Current Neuropharmacology Annexins as Neuroprotective Agents in the Central Nervous System
Current Medicinal Chemistry - Central Nervous System Agents The Relationship Between HIV Infection and Cardiovascular Disease
Current Cardiology Reviews Prion Protein Misfolding and Brain Degeneration
Current Medicinal Chemistry - Immunology, Endocrine & Metabolic Agents Neuroprotection by NMDA Receptor Antagonists in a Variety of Neuropathologies
Current Drug Targets Modeling Rett Syndrome Using Human Induced Pluripotent Stem Cells
CNS & Neurological Disorders - Drug Targets Mediterranean Diet and Risk of Dementia
Current Alzheimer Research Platelet Function in Inflammatory Diseases: Insights from Clinical Studies
Inflammation & Allergy - Drug Targets (Discontinued) Molecular Pathways Involved in Apoptotic Cell Death in the Injured Cochlea: Cues to Novel Therapeutic Strategies
Current Pharmaceutical Design Computational and In-Vitro Validation of Natural Molecules as Potential Acetylcholinesterase Inhibitors and Neuroprotective Agents
Current Alzheimer Research Principles and Applications of Diffuse Optical Imaging for the Brain
Current Medical Imaging On the Origin of Cortical Dopamine: Is it a Co-Transmitter in Noradrenergic Neurons?
Current Neuropharmacology