From: Insight into the emerging and common experimental in-vivo models of Alzheimer’s disease
S. No. | Animal model | Major pathology | Merits | Demerits | Method of administration /Dose | References |
---|---|---|---|---|---|---|
1. | Streptozotocin | Neuroinflammation Oxidative stress Biochemical modulations | Induces sporadic AD that is highly prevalent | Long term development of amyloid and tau pathologies No effect on contextual fear memory, High mortality | ICV/ 3 mg/kg | |
2. | Scopolamine | Cholinergic dysfunction | Different parameters can be evaluated therefore aids in developing multitarget therapy No Involvement of any surgical procedure | Do not completely mimic AD pathologies Mainly used for preventive AD treatments | ICV/ 2 mg/kg | |
3. | Colchicine | Tau hyperphosphorylation | Mimics sporadic AD pathologies Excitotoxicity can also be explored | High mortality Adverse effects | ICV/15 μg/5 μl Orally/0.3 mg/kg | |
4. | Okadaic acid | Tau hyperphosphorylation | Similar characteristic pathologies of AD Rapid disease induction | Side effects due to acting upon PP2A that is expressed throughout the body | ICV/70 ng/day | |
5. | Amyloid-β1-42 | Amyloid-β aggregation Neuroinflammation | Exhibit predictive, face, and construct validity | Neurofibrillary tangles are not seen Adult rodents are used instead of old ones | ICV/ 80 μmol/L Intrahippocampal/ 1 µg/µL | |
6. | Acrolein | Oxidative stress Neuroinflammation | Simulates multiple AD pathologies | Typical Aβ plaques as seen in AD individuals are not observed | Intragastric/ 2.5 mg/kg/day | |
7. | Heavy metals | Oxidative stress, Neurofibrillary tangles | Ease of aluminum administration Less mortality rates | Plaques pathology is different from AD in humans | Intraperitoneally/ 100 mg/kg Orally/ 150–300 mg/kg |