Alzheimer’s disease (AD) is a brain disorder characterized by slowly progressing dementia and irreversible damage to the brain.
Alzheimer’s Disease dementia
Alzheimer's disease is the most common type of dementia and affects memory, language, and thought. Patients with AD die on average after four to eight years after diagnosis, but can live as long as 20 years.
Prior to formal diagnosis there is a time period referred to as preclinical AD. During this preclinical stage, brain pathology is emerging and progressing slowly. Treatments for AD need to be started early, during the preclinical stage to avoid irreversible damage.
Pathology in the brain: amyloid and tau
The histopathological hallmarks of Alzheimer’s disease (AD) are extracellular plaques composed of amyloid beta (Aβ) and intracellular inclusions of the protein tau (neurofibrillary tangles).
Aβ aggregates are thought to underlie, at least in part, downstream pathology including tau misfolding, synaptic toxicity and inflammation. Tau pathology strongly correlates with neurodegeneration and cognitive deficits in AD. Both pathologies can be modeled in transgenic mice or by injection of viral vectors or aggregate-containing AD brain extracts.
Risk factors: APOE4
The largest genetic risk factor for late onset Alzheimer’s disease (AD) is genetic variation in the gene coding for Apolipoprotein E (APOE). Carriers of the APOE4 allele have a 3 to 12 fold increased risk to develop AD. APOE is a protein - expressed by astrocytes and microglia - that is involved in the metabolism of fats and neuroinflammation.
Mice with a humanized APOE4 are attractive models for testing APOE-targeting therapeutics. APOE models are also often crossed with amyloid or tauopathy mouse models, which exacerbates the phenotypes observed in these mice.
Sylics offers services with several different transgenic amyloid models, which recapitulate the plaque pathology of AD.
Sylics offers services with several different transgenic tau models, which recapitulate the neurofibrillary tangle pathology of AD.
Sylics uses an AD brain extract injection model, which provides a translational model of tau pathology seeding and spreading.
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