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TG (P301S) AD Model
The TG (P301S) Alzheimer's Disease (AD) Model is a widely recognized transgenic model used to study tau pathology in Alzheimer's disease and other tauopathies. The P301S mutation in the tau gene leads to the development of neurofibrillary tangles, a key pathological feature of AD. This model exhibits progressive tau aggregation, neuroinflammation, and neuronal loss, which mimic the neurodegenerative processes seen in human Alzheimer's disease. P301S mice show neurodegeneration and brain atrophy principally in the hippocampus that spreads to other regions in the brain. Behavioral phenotypes of this model include cognitive impairment and motor deficits that are associated with age.
Our latest validation data confirm the robust reproducibility of tau aggregation and its downstream effects, including neuronal dysfunction and cognitive decline, making this model a valuable tool for preclinical testing of tau-targeting therapies and other disease-modifying treatments in AD research.
TG (5xFAD) AD Model
The TG (5xFAD) Alzheimer’s Disease Model is an aggressive transgenic mouse model designed to replicate critical features of early-onset familial Alzheimer’s disease. It harbors five mutations linked to familial AD in the APP (amyloid precursor protein) and PS1 (presenilin 1) genes, leading to accelerated amyloid-beta plaque formation. These mutations include the Swedish (K670N/M671L), Florida (I716V), and London (V717I) mutations in APP, along with the M146L and L286V mutations in PSEN1.
Key pathological features appear early in this model:
- Intraneuronal amyloid-beta (Aβ) and extracellular plaques can be observed as early as 1.5 to 2 months in the brain and at 3 months in the spinal cord.
- There is an approximately 40% loss of layer V pyramidal neurons by one year of age, contributing to significant neurodegeneration.
- Microgliosis and astrogliosis, which are inflammatory responses, are associated with the presence of amyloid plaques, with microgliosis being linked to vascular damage.
Behavioral and cognitive deficits mirror the progression of AD:
- Impairments in spatial working memory emerge between 3 and 6 months, worsening with age.
- Progressive reductions in anxiety are observed during this period, with significant differences noted in tests like the open field test between transgenic and wild-type mice, particularly after 9 to 12 months.
- Sensorimotor deficits such as balance impairments are evident in 9-month-old mice during balance-beam tests.
This model is valuable for investigating amyloid-driven pathology and testing therapeutic interventions targeting early-onset Alzheimer’s.
β-amyloid-induced Cognitive Impairment AD model
The β-Amyloid-Induced Cognitive Impairment Model is a non-transgenic approach frequently used to study the direct effects of amyloid-beta on cognitive functions. In this model, synthetic β-amyloid peptides are administered into the brain of rodents, typically via intracerebroventricular (ICV) injection, to induce cognitive deficits and simulate certain pathological aspects of Alzheimer's disease (AD).
One of the hallmark features of AD is the accumulation of extracellular β-amyloid plaques, which can activate inflammasomes and trigger chronic neuroinflammation. This inflammatory response, along with amyloid plaque deposition, is thought to play a significant role in exacerbating cognitive decline. The β-amyloid ICV injection model is valuable for inducing cognitive impairments in rodent models, and it is commonly used to assess the efficacy of experimental therapies aimed at improving memory and cognitive performance.
This model is essential for preclinical testing, offering insights into the mechanisms of amyloid toxicity and helping evaluate potential therapeutic agents targeting amyloid-related cognitive decline.
Scopolamine-induced Cognitive Impairment AD Model
The Scopolamine-Induced Cognitive Impairment Alzheimer’s Disease (AD) Model is a pharmacological model commonly used to study memory deficits and cognitive decline. Scopolamine, an anticholinergic drug, temporarily impairs cholinergic neurotransmission by blocking muscarinic acetylcholine receptors in the brain. This disruption mimics the cholinergic deficits seen in Alzheimer's disease, as reduced acetylcholine activity is a key factor contributing to cognitive impairment in AD patients.
Key features of the model:
- Rapid Onset: Scopolamine administration results in acute, reversible cognitive impairment, making it useful for short-term studies.
- Memory Deficits: The model is particularly effective for inducing deficits in learning and memory, often tested using tasks such as the Morris water maze or passive avoidance tests.
- Cholinergic Dysfunction: By blocking muscarinic receptors, the model mimics the cholinergic system dysfunction seen in AD, allowing researchers to evaluate potential treatments that target cholinergic pathways.
The Scopolamine-Induced Cognitive Impairment Model is widely used in preclinical research to evaluate the efficacy of memory-enhancing drugs and other therapies aimed at improving cognitive function, particularly those targeting cholinergic signaling.
This model offers a fast and reliable way to assess potential treatments, though its short-term effects differ from the progressive nature of Alzheimer's disease seen in transgenic models.