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Table 2 Salient features of transgenic animal models of AD

From: Insight into the emerging and common experimental in-vivo models of Alzheimer’s disease

S. No

Model

Transgene

Transgenic promoter

Merits

Demerits

References

1.

PDAPP

APP

PDGF

High pathological similarity with AD patients

Difficulty in standardization and differentiating between functional and pathogenic Aβ

[80, 82, 83]

2.

APP23

APP751 cDNA

Neuron-specific murine Thy-1

Hippocampus and neocortex regions are majorly affected as observed in humans

Neurofibrillary tangles are not observed

[84, 85]

3.

Tg2576

APP

Hamster prion protein (PrP)

Slow rate of Aβ deposition

Scant Aβ pathology and plaque burden

[86, 92, 93]

4.

hAPP-J20 mice

Swedish (K670N and M671L);

(V7171F)

PDGF

High propensity for thigmotactic swimming thus better to evaluate spatial memory

Neuroinflammation and neuronal cell loss occur before Aβ pathology making it difficult to study plaque development

[95, 96, 99]

5.

P301S

PS19

Murine Thy1

Atrophy and damage of hippocampal region makes it clinically relevant to AD patients

No amyloid plaques

No link between genetic mutation and tau pathology is found in AD patients

[66, 100, 101]

6.

APP/PS1

APPswe, PS1dE9

Mouse prion protein

Amyloid plaque morphology is similar to humans

Homozygous lines are produced

Late onset of cognitive dysfunction

No signs of motor deficits

[105, 106, 135]

7.

3 × Tg or LaFerla mouse

APP, PSEN1, MAPT tau

Mouse Thy1 minigene

Both amyloid plaques and tau tangles can be seen

Evaluation is challenging due to multiple gene stimulation

[107, 110, 112]

8.

5 × FAD

Swedish (K670N, M671L), Florida (I716V), and London (V7171) and human PSEN1 (M146L and L286V) regulated by Thy1 promoter

Thy1 promoter

Prominent amyloid plaque deposition similar to AD patients

No tau pathology is observed

[113, 114]