With the endogenous Cx3cr1 locus, CX3CR1-GFP mutant can have detectable EGFP expression in brain microglia, dendritic cells, NK cells, and monocytes so that those cells can be visualized and traced.

As even the homozygous mutant are fertile, viable with normal size, and exhibit no gross physical or behavioral abnormalities. Instead of a disease model, CX3CR1-GFP might be better considered as a tool model for the investigation of leukocyte migration, trafficking and transplantation.

This disease model possess three mutations alleles, APPSwe, Psen1, and tauP301L. The APPSwe and Psen1 affect the beta-secretase and gama-secretase respectively, which would therefore induce the amyloidosis pathologies, such as both the intra- and extracellular Aβ deposition, together. 

The tauP301L, on the other hand, can induce the aggregation of 4R tau protein and thereby induce the tauopath, mainly in hippocampus and cortex, of the model. 

Together, the three mutations recapitulate both the tauopathy and amyloid pathologies in AD and can thereby be used as a more comprehensive disease model to study the inter-relationship between those two pathologies and their joint effect to the disease progression and pathologies, ranging from LTP deficits to synaptic transmission impairment, from cognitive deficits to gliosis.

DBA/2J possesses various mutations contributing to its pathologies in audition and vision.

For audition, there are Cdh23ahl, asp2 mutation and also 3 more recessive alleles, together they induce various auditory pathologies, ranging from high-frequency hearing loss to cochlear pathologies, from neurodegeneration to audiogenic seizures.

For vision, there are Tyrplisa and GpnmbR150X alleles, together they induce various visual pathologies, especially in iris and IOP, that closely resemble human hereditary glaucoma.

Moreover, DBA/2J also exhibit characteristic susceptibility to various pathological states, such as atherosclerotic aortic lesions and calcareous pericarditis, and to various chemical substances, ranging from alcohol to morphine, from haloperidol to phytohemagglutinin.

All these characteristic make DBA/2J a versatile animal model for various research field, ranging from neurobiology to sensorineural research.

Carrying the rd10 mutation in Pde6b gene, B6.CXB1-Pde6brd10/J would have abnormality in the β subunit in their phosphodiesterase (PDE), which is a peripheral membrane enzyme participating in the phototransduction cascade of rod photoreceptors. Therefore, this transgenic moel would experience various retinal pathologies, especially in the photoreceptor population in the outer nuclear layer, such as the progressive degeneration in rod photoreceptor and progressive decrement in rod and cone ERG a- and b- waves.

The pathological phenotype induced by the mutation mimick retinitis pigmentosa and it has a later onset and milder severity than other model such as rd1, it might be a suitable experimental drug therapy model for retinitis pigmentosa.

 Poccessing five transgenic mutation, 5XFAD have drastically different gene expression (1300 differentially expressed gene at 4 months) compared to wild type. Three mutation are on APP and two mutations are on PS1, together they grant 5XFAD huge production rate of Aβ42, which is a highly amyloidogenic and thus can lead to severe amyloid pathology in various regions in CNS, ranging from subiculum to cortical layer V, from hippocampus to thalamus, etc. 

   Amyloid pathology in 5XFAD is associated with astrogliosis and microgliosis, and the later is in turn linked with microvascular damage, which is another angiopathy linked with amyloidosis beside the progressive cerebral amyloid angiopathy (CAA).

   Worse still, amyloidosis in 5XFAD is also linked with neurites dystrophy, ranging from axonal abnormality to progressive myelin abnormalities, which might be the underlying cause for the synaptic dysfunction in 5XFAD, ranging from decrement in excitability to even synapse loss.

   The synaptic dysfunction might in turn be the reason for the neurodegeneration, especially in cortical layer V, which experience up to about 40% neuronal loss.

   Reasonably, the severe neurodegeneration in 5XFAD might be the cause of its cognitive dysfunction, including progressive working memory deficits and decrement in anxiety, and behavioral dysfunction, including sensorimotor impairments and aberrant reflexes.

   Tauopathy, on the other hand, is not known in 5XFAD.

   Therefore, all in all, 5XFAD might be a great AD model to isolate its amyloid pathology out, amplify and then investigate into its effects within a short time span

• APP/PS1 possess two mutations, APP Swedish and Psen1, which can affect the β- and γ-secretase respectively and thereby increase the production and thus aggregation of Aβ40 and Aβ42. Therefore, together they can induce severe amyloidosis and hence amyloid pathologies in brain regions ranging from hippocampus to cortex, from amygdala to cerebellum.
• Moreover, the amyloid plaque are implicated with various other pathologies, ranging from astrogliosis to microgliosis, from angiopathy to retinopathy.
• synaptic dysfunctions such as neurite dystrophy were also observed, and may contribute to the cognitive deficits of APP/PS1 such as memory and learning impairments.
• Transcriptomic analysis also reveals genes differentially expressed between APP/PS1 and wild type.
• Nonetheless, there is no neuronal loss observed up to 12 months.
• Moreover, the amyloid pathologies of APP/PS1, such as amyloid deposition in cerebellum and peripheral Aβ in plasma, exhibit significant sexual dimorphism patterns, which are mostly female-biased.
• On the other hand, as for the tauopathy, although there is observed immunoreactivity of phospho-tau epitopes in CA3 hippocampal neurons at late stage(16 months), neurofibrillary tangle is not observed in APP/PS1.
• Apart from the classical AD pathologies, Seizure problem also exist in some strain with specific genetic background.