App/ps1 Mice
App/ps1 Mice - Related Videos
05:40
Using an Automated Hirschberg Test App to Evaluate Ocular Alignment
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Cited by 9 •
2020
We present a protocol of using a smartphone app to perform Hirschberg test for measuring manifest and intermittent ocular misalignment (strabismus) under near and far fixation conditions.
07:55
Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
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Cited by 6 •
2015
While the transport of cell surface proteins is relatively easily studied, visualizing the trafficking of intracellular proteins is much more difficult. Here, we use constructs incorporating photoactivatable GFP and demonstrate a method to accurately follow the amyloid precursor protein from the Golgi apparatus to down-stream compartments and follow its clearance.
17:45
T-maze Forced Alternation and Left-right Discrimination Tasks for Assessing Working and Reference Memory in Mice
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Cited by 94 •
2012
This article presents the protocol of T-maze tests using a modified automated apparatus for assessing the learning and memory functions in mice.
19:32
Contextual and Cued Fear Conditioning Test Using a Video Analyzing System in Mice
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Cited by 148 •
2014
This article presents a protocol for a contextual and cued fear conditioning test using a video analyzing system to assess fear learning and memory in mice.
06:17
Measuring the Strength of Mice
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Cited by 287 •
2013
Deficits in muscular strength occur in many clinical conditions such as motor neuron disease. The inverted screen and weight lifting tests described here measure strength in mice almost exclusively, with minimal influence of factors such as coordination.
FAQs
Co-expression of mutant human APP and PS1 increases amyloid-β production, which promotes progressive aggregation in the brain. Over time, accumulated amyloid-β forms cerebral plaques that provide a pathological context for examining downstream changes, including impaired synaptic function, neuroinflammation, neuronal damage, and altered learning and memory.
Amyloid pathology can be examined alongside changes in communication between neurons and inflammatory responses in the brain. Measuring synaptic dysfunction and neuroinflammation helps researchers connect plaque accumulation with functional and cellular consequences rather than treating plaques as the only outcome. This supports a broader analysis of how Alzheimer’s-related pathology affects brain function.
Because amyloid-β aggregation and plaque development occur over time, the timing of assessment can influence which pathological or functional changes are observed. Investigators can therefore examine relationships among progressive amyloid pathology, neuronal damage, inflammation, synaptic dysfunction, and memory-related changes, while also considering how closely those findings reflect mechanisms of human Alzheimer’s disease.
Studies can evaluate several linked outcome categories, including cerebral plaques, synaptic dysfunction, neuroinflammation, neuronal damage, and performance in learning and memory tasks. Using these complementary measures allows investigators to compare structural or pathological changes with brain function. The resulting profile can help characterize disease-related effects and judge whether an intervention changes more than amyloid accumulation alone.
Investigators use this model to evaluate anti-amyloid therapies, imaging approaches, and other interventions before further development. Treatment studies can examine whether an approach affects amyloid pathology or associated outcomes such as inflammation, neuronal damage, synaptic dysfunction, learning, or memory. This makes the mice useful for linking experimental interventions with measurable disease-related changes.
The model provides a way to study how amyloid pathology relates to brain function in an experimental system. Its usefulness extends beyond plaque assessment because researchers can investigate cellular, neural, behavioral, therapeutic, and imaging outcomes together. At the same time, findings must be evaluated in relation to how closely the model reflects human disease mechanisms.