Object recognition tasks detect cognitive deficits in transgenic Alzheimer's disease (AD) mouse models. Object recognition, however, is not a unitary process, and there are many uncharacterized facets of object processing with relevance to AD. We therefore systematically evaluated object processing in 5xFAD and 3xTG AD mice to clarify the nature of object recognition-related deficits. Twelve-month-old male and female 5xFAD and 3xTG mice were assessed on tasks for object identity recognition, spatial recognition, and multisensory object perception. Memory and multisensory perceptual impairments were observed, with interesting dissociations between transgenic AD strains and sex that paralleled neuropathological changes. Overreliance on the widespread "object recognition" task threatens to slow discovery of potentially significant and clinically relevant behavioural effects related to this multifaceted cognitive function. The current results support the use of carefully designed object-based test batteries to clarify the relationship between "object recognition" impairments and specific aspects of AD pathology in rodent models.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329782 | PMC |
| http://dx.doi.org/10.1038/s41598-018-37312-0 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Anti-neuroinflammatory and Neuroprotective Effects of T-006 on Alzheimer's Disease Models by Modulating TLR4-Mediated MyD88/ NF-κB Signaling.
CNS Neurol Disord Drug Targets
January 2025
School of Medicine, Foshan University, Foshan, 528000, China.
Introduction: Neuroinflammation derived from the activation of the microglia is considered a vital pathogenic factor of Alzheimer's Disease (AD). T-006, a tetramethylpyrazine derivative, has been found to alleviate cognitive deficits via inhibiting tau expression and phosphorylation in AD transgenic mouse models. Recently, T-006 has been proven to dramatically decrease the levels of total Amyloid β (Aβ) peptide and Glial Fibrillary Acidic Protein (GFAP) and suppress the expression of ionized calcium binding adaptor molecule-1 (Iba-1) in APP/PS1 mice.
View Article and Find Full Text PDFEffect of Dietary Ketosis and Nicotinamide Riboside on Hippocampal Krebs Cycle Intermediates and Mitochondrial Energetics in a DNA Repair-Deficient 3xTg/POLβ Alzheimer Disease Mouse Model.
J Neurochem
January 2025
The Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, USA.
Alzheimer disease is a neurodegenerative pathology-modifying mitochondrial metabolism with energy impairments where the effects of biological sex and DNA repair deficiencies are unclear. We investigated the therapeutic potential of dietary ketosis alone or with supplemental nicotinamide riboside (NR) on hippocampal intermediary metabolism and mitochondrial bioenergetics in older male and female wild-type (Wt) and 3xTgAD-DNA polymerase-β-deficient (3xTg/POLβ) (AD) mice. DNA polymerase-β is a key enzyme in DNA base excision repair (BER) of oxidative damage that may also contribute to mitochondrial DNA repair.
View Article and Find Full Text PDFNose-to-brain delivery of DHA-loaded nanoemulsions: A promising approach against Alzheimer's disease.
Int J Pharm
January 2025
MMDN, University of Montpellier, EPHE, INSERM, Montpellier, France; LipSTIC LabEx (ANR-11-LABX0021), Dijon, France. Electronic address:
Reduced docosahexaenoic acid (DHA) concentrations seem to be associated with an increased risk of Alzheimer's disease (AD), and DHA accretion to the brain across the blood-brain-barrier (BBB) can be modulated by various factors. Therefore, there is an urgent need to identify an efficient and non-invasive method to ensure brain DHA enrichment. In the present study, a safe and stable DHA-enriched nanoemulsion, designed to protect DHA against oxidation, was designed and administered intranasally in a transgenic mouse model of AD, the J20 mice.
View Article and Find Full Text PDFShenghui decoction inhibits neuronal cell apoptosis to improve Alzheimer's disease through the PDE4B/cAMP/CREB signaling pathway.
Phytomedicine
January 2025
Collaborative Innovation Center of Prevention and Treatment of Major Diseases by Chinese and Western Medicine, Henan Province, Henan University of Chinese Medicine, Zhengzhou 450046, Henan, China; Collaborative Innovation Center of Research and Development on the whole Industry Chain of Yu-Yao, Henan University of Chinese Medicine, Zhengzhou 450046, Henan, China. Electronic address:
Background: Shenghui Decoction (SHD) is a frequently utilized traditional Chinese medicine formula in clinical settings for addressing cognitive impairment in elderly individuals. Nevertheless, the precise mechanism by which SHD exerts its effects on the most prevalent form of dementia, Alzheimer's disease (AD), remains to be elucidated.
Methods: Temperature-induced transgenic C.
Comprehensive Approach for Sequential MALDI-MSI Analysis of Lipids, -Glycans, and Peptides in Fresh-Frozen Rodent Brain Tissues.
Anal Chem
January 2025
Department of Pharmaceutical Biosciences, Spatial Mass Spectrometry, Science for Life Laboratory, Uppsala University, SE-75124 Uppsala ,Sweden.
Multiomics analysis of single tissue sections using matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) provides comprehensive molecular insights. However, optimizing tissue sample preparation for MALDI-MSI to achieve high sensitivity and reproducibility for various biomolecules, such as lipids, -glycans, and tryptic peptides, presents a significant challenge. This study introduces a robust and reproducible protocol for the comprehensive sequential analysis of the latter molecules using MALDI-MSI in fresh-frozen rodent brain tissue samples.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!