Repeated multi-domain cognitive training prevents cognitive decline, anxiety and amyloid pathology found in a mouse model of Alzheimer disease.

Education, occupation, and an active lifestyle, comprising enhanced social, physical, and mental components are associated with improved cognitive functions in aged people and may delay the progression of various neurodegenerative diseases including Alzheimer's disease. To investigate this protective effect, 3-month-old APP mice were exposed to repeated single- or multi-domain cognitive training. Cognitive training was given at the age of 3, 6, & 9 months.

Hippocampal damage causes retrograde amnesia for objects' visual, but not odour, properties in male rats.

Damage to the hippocampus produces profound retrograde amnesia, but odour and object discrimination memories can be spared in the retrograde direction. Prior lesion studies testing retrograde amnesia for object/odour discriminations are problematic due to sparing of large parts of the hippocampus, which may support memory recall, and/or the presence of uncontrolled, distinctive odours that may support object discrimination. To address these issues, we used a simple object discrimination test to assess memory in male rats.

Weak-hyperactive hippocampal CA1 neurons in the prodromal stage of Alzheimer's disease in hybrid App × Thy1-GCaMP6s mice suggest disrupted plasticity.

This study investigated the impact of familial Alzheimer's disease (AD)-linked amyloid precursor protein (App) mutations on hippocampal CA1 neuronal activity and function at an early disease stage in App × Thy1-GCaMP6s (A-TG) mice using calcium imaging. Longitudinal assessment of spatial behavior at 12 and 18 months of age identified an early disease stage at 12 months when there was significant amyloid beta pathology with mild behavioral deficits. Hippocampal CA1 neuronal activity and event-related encoding of distance and time were therefore assessed at 12 months of age in several configurations of an air-induced running task to assess the dynamics of cellular activity.

Dramatic impacts on brain pathology, anxiety, and cognitive function in the knock-in APP mouse model of Alzheimer disease following long-term voluntary exercise.

Background: An active lifestyle is associated with improved cognitive functions in aged people and may prevent or slow down the progression of various neurodegenerative diseases including Alzheimer's disease (AD). To investigate these protective effects, male APP mice were exposed to long-term voluntary exercise.

Methods: Three-month-old AD mice were housed in a cage supplemented with a running wheel for 9 months for long-term exercise.

The effect of Aβ seeding is dependent on the presence of knock-in genes in the mice.

Alzheimer's disease (AD) is characterized by the prion-like propagation of amyloid-β (Aβ). However, the role of Aβ in cognitive impairment is still unclear. To determine the causal role of Aβ in AD, we intracerebrally seeded the entorhinal cortex of a 2-month-old mouse model with an Aβ peptide derived from patients who died from rapidly progressing AD.

Intracerebral seeding of amyloid-β and tau pathology in mice: Factors underlying prion-like spreading and comparisons with α-synuclein.

Alzheimer's disease (AD) is characterized neuropathologically by progressive neurodegeneration and by the presence of amyloid plaques and neurofibrillary tangles. These plaques and tangles are composed, respectively, of amyloid-beta (Aβ) and tau proteins. While long recognized as hallmarks of AD, it remains unclear what causes the formation of these insoluble deposits.

Age-dependent behavioral and biochemical characterization of single APP knock-in mouse (APP) model of Alzheimer's disease.

Saito et al developed a novel amyloid precursor protein (APP) knock-in mouse model (APP) for Alzheimer's disease (AD) to overcome the problem of overexpression of APP in available transgenic mouse models. However, this new mouse model for AD is not fully characterized age-dependently with respect to behavioral and biochemical changes. Therefore, in the present study, we performed an age-dependent behavioral and biochemical characterization of this newly developed mouse model.