Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) plaques, tau neurofibrillary tangles, and age-related cognitive decline. At Ace Therapeutics, we specialize in aged rodent models of Alzheimer's disease, bridging the gap between preclinical research and clinical translation. Our models replicate the complexities of late-onset AD, offering researchers a robust platform to study neurodegeneration, test therapeutics, and validate biomarkers.
Late-onset Alzheimer's disease, which accounts for over 95% of cases, is intrinsically linked to aging. Traditional transgenic models often focus on early-onset familial mutations, failing to fully capture age-associated pathologies like oxidative stress, chronic neuroinflammation, and vascular dysfunction. Aged rodent models address this gap by naturally developing AD-like features, including
These models are critical for studying sporadic AD and evaluating therapies targeting age-related mechanisms.
We utilize C57BL/6 mice and rats aged 18–24 months, coupled with dietary or genetic interventions, to accelerate AD-related pathology.
Robust validation ensures translational relevance.
Our aged models are optimized for evaluating diverse interventions
Aged rodents exhibit chronic microglial activation and cytokine dysregulation, mirroring human AD.
Aging exacerbates vascular contributions to AD.
Our models are trusted for
Partner with Ace Therapeutics to leverage aged rodent models that mirror the complexity of human Alzheimer's disease. Contact us to design a study tailored to your preclinical goals.
Why choose aged models over young transgenic mice for AD research?
Aged models naturally develop multifactorial pathologies (e.g., neuroinflammation, vascular dysfunction) seen in human late-onset AD, offering higher translational relevance.
How long does it take to induce AD-like phenotypes in aged rodents?
Depending on the protocol, metabolic or vascular challenges require 12–24 weeks, while combined interventions may accelerate pathology to 8–12 weeks.
Can these models replicate cognitive decline?
Yes. Our behavioral assays consistently detect age-related deficits in spatial memory and learning.
What endpoints are measured in therapeutic studies?
We assess cognitive performance, Aβ/tau burden, synaptic integrity, and inflammatory markers. Custom endpoints (e.g., proteomics) are also available.
Do you offer models for comorbid conditions like diabetes or hypertension?
Yes. We integrate metabolic syndrome or hypertension induction to study AD comorbidities.
Our products and services are for research use only and can not be used for diagnostic or other purposes.
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Ace Therapeutics is a specialized team of scientists and technical professionals committed to working closely with clients worldwide. We offer comprehensive preclinical testing solutions to support the development of novel therapies and medications across a range of disease areas.