Elevated Aβ peptides accumulating into plaques starting at 6 months. Microgliosis and astrocytosis, especially around plaques. Reduced synaptophysin and PSD-95 indicative of synaptic loss. No tangle pathology or neurodegeneration.
Memory impairment by 18 months as measured by the Y maze. No significant impairment in the Morris water maze.
Yes
C57BL/6
Apptm2.1Tcs/Apptm2.1Tcs
No overexpression of APP. Generates wild-type levels of AICD.
Aggressive amyloidosis with deposition in the cortex beginning at 2 months and approaching saturation by 7 months. Aβ deposition in heterozygous mice at 4 months. Subcortical amyloidosis. Exacerbated microgliosis and astrocytosis compared to APPNL-F mice. Reduced synaptophysin and PSD-95 indicative of synaptic loss. No tangle pathology or neurodegeneration.
Memory impairment by 6 months as measured by the Y maze.
Yes
C57BL/6
Apptm3.1Tcs/Apptm3.1Tcs
No overexpression of APP. Wild-type levels of AICD.
Plaques start in the subiculum, spreading to the frontal cortex as dense and diffuse aggregates. Prominent amyloid deposits in brain vessels after 15 months. Microbleeds. Amyloid-associated inflammation. CSF Aβ42/Aβ40 ratio decreases from 15 months. Dystrophic neurites containing hyperphosphorylated tau, but no tangle pathology.
From the age of 6 months, spatial and non-spatial orientation and memory deficits by Morris water maze. Impaired associative learning. Increased agitation/anxiety from 8 weeks. Reduced ambulation, especially with age. Hyperactivity and aggression.
Yes
Originally generated on FVB/N background; available at reMYND as C57BL/6xFVB/N
Tg(Thy1-APPLon)2Vln/0
Increased mortality (72% by day 180). Increased incidence of seizures.
Available through the KU Leuven Research and Development Office; the CRO reMYND offers research services with this line.
Robust early plaque development (by 3 months in homozygotes, 5 months in hemizygotes), predominantly congophilic dense-core amyloid plaques surrounded by dystrophic neurites and gliosis. Some diffuse plaques and cerebral amyloidosis. No tau tangles. Neurons have reduced dendritic length, surface area, and branches.
Age-related learning and memory deficits, especially episodic memory, in select paradigm-specific tasks by 12 months.
Yes
Co-injection of transgenes into B6CBF1 oocytes, back-crossed to C57BL/6
B6;CB-Tg(Thy1-PSEN1*M146V/Thy1-APP*swe)10Arte
Good breeding capabilities and no premature death.
Amyloid plaques in the hippocampus, cerebral cortex. Gliosis. Dystrophic neurites. Decreased synaptic and dendritic density in the hippocampus.
Deficits in a variety of memory paradigms from a young age. Deficits in the radial arm maze at 3 months (before plaques), object recognition, operant learning, spatial reference memory (starting at 3-4 months), cued fear conditioning at 11 months.
Yes
C57B6 x DBA2
Alterations in sleep/wake states, thermoregulation, and motor activity.
Age-related accumulation of Aβ in the hippocampus and cortex leading to plaque deposition by 12 months of age. Early gliosis and dystrophic neurites, not limited to the vicinity around plaques. Changes in synaptic morphology and number, along with increased number of lysosomes.
Deficits in spatial memory prior to Aβ deposition, including deficits in the Morris water maze by 6 months Deficits in spontaneous alternation behavior in the Y maze by 12 months. No deficit in fear conditioning.
Yes
Transgene injected into C57BL/6 x C3H oocytes, some backcrossing to C57BL/6
No differences in body temperature, locomotor activity, or Rotarod performance, relative to non-Tg controls.
Aβ deposits beginning at 3 months of age, with fibrillar plaques by 6 months in the cerebral cortex and hippocampus. Some vascular amyloid. Plaques surrounded by dystrophic neurites and reactive glia. No tangles or neuronal loss. Female mice have more rapid and severe amyloid pathology.
Age-dependent impairment in object recognition memory starting around 6 months of age.
Yes
TAS10 transgene originally injected into C57BL/6 x C3H oocytes, with some backcrossing to C57BL/6. TPM generated on pure C57BL/6 background.
Abundant pre-tangle pathology, but only rare mature tangles, and only at advanced ages. Tau pathology included mislocalization of tau to the somatodendritic compartment, aggregation, and hyperphosphorylation.
Numerous parenchymal Aβ plaques by 11-13 months with some vascular amyloid. Oxidative lipid damage, astrogliosis and microgliosis. No tangles or neuronal loss.
Impaired spatial learning, working memory, and contextual fear conditioning reported at <6 months although other studies have reported normal cognition at this age with progressive impairment by >12 months.
Yes
B6;SJL Mixed Background
B6;SJL-Tg(APPSWE)2576Kha
Between 7 -12 weeks males become aggressive and begin to fight. Premature mortality: mortality of >20% anticipated, particularly in males.