Table 7.

In vivo AD models in some mammal species.

Non-Mammalian AD Models
Models	Model Type	Advantages	Pitfalls	References
Rabbits	Interventional	Induction of AD-pathology after brain injection of aluminum maltolate (features: amyloid aggregation, NFT formation and neurodegeneration). Non aggressive animal.	The structure of NFTs is different from human.	[215,216]
Octodon Degus	Natural	Development of AD-like disease with age. Aβ accumulation and plaque formation, with age. Tau accumulation. Memory impairments.	Inconsistensy from one study to another. Lack of appropriate brain map.	[92,218,219,220]
Dogs	Natural	Development of AD-like disease with age (Aβ plaques and cognitive deficits).	Diffuse plaques contrary to compact human plaques. No NFTs but pretangles. No cholinergic deficit. Long and variable lifespan. Lack of consistency.	[92,220]
Non human Primates (NHPs)	Natural	Development of AD-like disease with age. Genetically and anatomically closest animal to human (example: 100% homology in Aβ sequence). Well-characterized, complex, and quantifiable behaviors. Four groups of NHPs with different specificities. Similar AD symptoms: Aβ accumulation and amyloid plaque formation in the brain.	Ethical concerns. Long lifespan. Costly, few animals. Do not perfectly reproduce the human disease (often develop diffuse amyloid plaques instead of compact plaques, some primates have NFTs and others do not, mild cognitive deficits rather similar to normal ageing than to AD-induced cognitive impairments). Inter individual variability.	[3,92]