Atherosclerosis |
Apoe-/-
|
High cholesterol levels |
[169] |
Increased sensitivity to fat and cholesterol-based dietsExtensive atherosclerosis by 3 months |
Ldlr-/-
|
Plaque development only in high fat diets |
[169,170] |
Better mimics human pathogenesis (lipoprotein profile) |
Atherosclerosis induction by 6 months |
Apoe-/- + Ldlr-/-
|
More severe atherosclerosis than Apoe-/- and Ldlr-/- individual knockouts |
[169] |
Lipoprotein profile similar to Apoe-/-
|
Ischemia |
Suture occlusion of artery |
Depends on which affected tissue is being modelled |
[171,172] |
Stroke |
Suture to occlude the middle cerebral artery |
Infarction (size dependent on occlusion time, suture size, suture material, etc.) |
[172] |
Striatum blood flow normalizes after 2 h |
Cortical blood flow remains low |
Endothelin-1 injection directly to middle cerebral artery |
Infarction (size dependent on dose) |
[172] |
Reduced cerebral blood flow–reperfusion takes hours |
Microsphere insertion into the middle cerebral artery |
Infarction (size dependent on microsphere size, material) |
[172] |
Alzheimer’s |
App-Indiana mutation with PDGF promoter |
18× APP RNA |
[173,174] |
10× APP protein |
Amyloid deposition |
apparent at 9 months |
Cerebral amyloid angiopathy |
App-Swedish mutation with hamster prion protein promoter |
5× APP protein |
[9,173,175] |
Amyloid deposition apparent at 11–13 months |
Cerebral amyloid angiopathy |
App-Swedish + Indiana mutation with hamster prion protein promoter |
Amyloid deposition apparent at 3 months |
[173,176] |
Cerebral amyloid angiopathy |
Parkinson’s |
Snca-a53t mutation with mouse prion protein promoter |
Initial motor control degradation and α-Syn inclusions at 8 months |
[177] |
Snca-a30p mutation with hamster prion protein promoter |
Initial motor control degradation at 13 months |
[178] |
Snca-e46k mutation with mouse prion protein promoter |
Initial motor degradation at 16 months |
[179] |
Slower disease progression than other mutations |