No transgene-related deficits seen in Morris water maze 4, 12, 21, 24 months of age or fixed consecutive number test 23 months of age. Gliosis and hyperphosphorylated tau in the vicinity of dense-core plaques. Fibrillar oligomeric species, e. No transgene-related deficits seen in Morris water maze 4, 12, 21, 24, months of age or fixed consecutive-number 23 months of age tests. By 18 months of age, Gallyas silver-positive staining is observed, indicative of paired helical filaments.
This is followed by thioflavin-S staining at 24 months. Neuronal loss is detectable by 24 months of age in areas with transgene expression e. Significant neuronal loss was not observed at 21 months de Calignon et al. Microglial activation and astrogliosis by 24 months of age, in conjunction with axonal degeneration and neuronal loss de Calignon et al. By 24 months of age pre- and post-synaptic densities were reduced in the middle third of the molecular layer of the dentate gyrus as measured by synapsin-1 and PSD staining de Calignon et al.
At 16 months of age, subtle differences in electrophysiological properties have been observed in the perforant pathway, including a decrease in LTP and an increase in the probability of neurotransmitter release Polydoro et al. Very mild and specific deficits in contextual fear conditioning at 16 months of age, but no deficits in the radial arm maze Polydoro et al.
Propagating tau pathology starting in the entorhinal cortex and spreading to regions functionally connected to the EC e. Neurodegeneration and axonal degeneration, first in EC and parasubiculum. Gliosis and synaptic loss. Subtle cognitive deficit in contextual fear conditioning, but not in the radial arm maze, at 16 months. Mild specific deficit in locomotor activity in the open field test. Pretangles as early as 2. Argyrophilic tangle-like inclusions in cortex by 4 months and in hippocampus by 5. Progressive loss of neurons and brain weight in 7 and 8. Gross atrophy of the forebrain by 10 months.
Retention of spatial memory Morris Water Maze became impaired from 2. No significant motor impairments up to 6 months. Spatial memory improved when transgene suppressed by dox. The number of CA1 neurons stabilized after a brief six to eight week suppression of transgenic tau. Spatial memory impairments by 2. No significant motor impairment up to 6 months of age. When the transgene was suppressed with dox at 2.
TAS10 mice initially have more synapses than non-Tg mice; specifically, greater numbers of synapses per neuron were documented at 12 and 18 months of age. However, by 24 months of age, TAS10 mice have fewer synapses than non-Tg mice. Deficits in spatial learning present by 6 months of age as measured by the Morris water maze. No difference from non-Tg at 2 months of age. Deficits in Y maze at 12 months. No deficit in fear conditioning up to 24 months of age. Qualitative difference in neuronal numbers at 24 months in specific regions of the hippocampus, but no significant neuronal loss.
At 12 to 14 months of age, deficits in basal synaptic transmission have been observed in the CA1 region, but short- and long-term synaptic plasticity are relatively normal Brown et al. Early gliosis and dystrophic neurites, not limited to the vicinity around plaques. Changes in synaptic morphology and number, along with increased number of lysosomes.
No deficit in fear conditioning. Some vascular amyloid is also observed. Plaque pathology is more severe in female mice. Greater numbers of reactive astrocytes and microglia by 6 months of age in the hippocampus and cortex, predominantly near amyloid plaques. Age-dependent impairment in object recognition memory starting around 6 months of age for both sexes.
No impairment at 3 to 4 months of age. Minimal neuronal loss up to 10 months of age. Some signs of loss in the immediate vicinity of plaques in the hippocampus Howlett et al. Some vascular amyloid. Plaques surrounded by dystrophic neurites and reactive glia. Female mice have more rapid and severe amyloid pathology.
Abnormally phosphorylated tau detected at two months and by eight months tau was mislocalized and misfolded and dystrophic neurites were observed. Tangle-like structures observed in the hippocampus by 14 months. At 14 months synapsin1 protein levels were decreased but synaptophysin levels remained at wild-type levels.
In the Morris water maze, Tau35 had the same performance as wild-type animals at six months but developed progressive deficits by eight months. Cell death was not formally assessed, however, overt neuronal death was not seen in the hippocampus. Progressive tau pathology in the hippocampus, including abnormally phosphorylated and misfolded tau, mislocalized tau, and tangle-like structures.
Impaired spatial learning and memory in the Morris water maze. Early motor impairments, including abnormal limb clasping, Rotarod deficits and decreased grip strength. Deficits in spatial learning and memory as indicated by performance in the Barnes maze at multiple time points 3, 6, 11 months of age. Absence of mature neurofibrillary tangles, but extensive pretangle pathology throughout the brain e. Extensive pretangle pathology throughout the brain e. Dystrophic neurites and axonal pathology spheroids. No overt neuronal loss. Motor deficits develop with age, including decreased grip strength and impaired Rotarod performance.
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Cognitive deficits, indicative of impaired spatial learning and memory, as assessed by the Barnes maze. Gallyas silver-positive intracellular inclusions of hyperphosphorylated tau aggregates in the entorhinal cortex at 15 months, and in the hippocampus and cerebral cortex at 24 months, but not at 18 months. Significant loss of NeuN-positive neurons in layer II of the entorhinal cortex at 15 months, and in the hippocampal CA1 region at 24 months, compared with non-Tg controls. No difference in the hippocampus at 18 months.
Reduced synaptic density at 6 months of age in select hippocampal areas compared to non-Tg mice and those expressing wild-type human tau. Densities in other areas were comparable until later ages i. Some changes in basal synaptic transmission and significant impairment of LTP evident by 6 months of age in some regions of the hippocampus.
Deficits in spatial reference memory by 6 months of age as measured by the Morris water maze. No difference from non-Tg littermates at 4 months of age. Aggregated tau in neurons of the entorhinal cortex, hippocampus, and cerebral cortex at advanced ages. Intraneuronal accumulation of tau oligomers in the hippocampus. Neuronal loss in the entorhinal cortex and hippocampus. Some hippocampal areas affected by age-related synaptic dysfunction and reduced synaptic density.
Reduced levels of synaptic proteins as early as 1. Further reductions in 3 and 6-month-old animals. Learning and memory impairments as early as 1. Neurofibrillary tangles were not observed; however, hyperphosphorylated tau occurred early in the form of oligomers and aggregates. No significant cell loss or astrogliosis in the brain. Age-dependent reduction in synaptic proteins e. Hyperphosphorylated tau oligomers and aggregates. Learning and memory deficits by 1. No significant motor impairment. This includes mislocalization of tau to the somatodendritic compartment, conformational changes indicative of aggregation, and hyperphosphorylation e.
Ser , Ser Electron microscopy showed a moderate decrease in spine synapses in the CA1 region of the hippocampus following 13 months of gene expression. 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.
Hyperphosphorylation, conformational changes, and aggregation of tau resulting in tangle-like pathology by 8 months. Age-associated deficit in two cognitive tests that do not depend heavily on motor ability, the passive avoidance task significant deficit starting at 5 months, but not 2 or 3 months of age and a novel object recognition task significant deficit at 9 months, but not at 2, 3, 5, or 7 months of age Maurin et al. Unknown at advanced age. Young mice months have a significantly higher spine maturation index than controls. At months, the spine maturation index remains high in the hippocampus, but is reduced to control levels in the cortex.
Pathologic hyperphosphorylation and conformational change of parenchymal tau in brain tissues starting at 7 months. Tangle-like pathology is mainly observed in the brain stem and spinal cord, and to a lesser extent in the midbrain and cerebral cortex. Age-dependent increase in total tau in CSF. Age-associated deficits in a passive avoidance task starting at 5 months and a novel object recognition task starting at 9 months. Progressive motor impairment and reduced activity, accompanied by increased clasping of hind and then forelimbs around seven months.
Neurofibrillary tangles in the neocortex, amygdala, hippocampus, brain stem and spinal cord at six months with progressive accumulation Yoshiyama et al. Neuron loss in the hippocampus and entorhinal cortex by nine to12 months, as well as in the amygdala and neocortex becoming more severe by 12 months Yoshiyama et al. Microgliosis at three months, especially in the white matter of the brain and spinal cord. Increased microgliosis by six months in white and gray matter of the hippocampus, amygdala, entorhinal cortex, and spinal cord. Microglial activation precedes astrogliosis Yoshiyama et al.
Synaptophysin immunoreactivity decreased progressively from three to six months in the CA3 region of the hippocamus. Impaired synaptic function Yoshiyama et al. Altered basal synaptic transmission smaller fiber volley amplitude, fEPSP slopes, and amplitudes Yoshiyama et al. Impairments in spatial learning and memory ability in the Morris water maze in six-month-old animals Takeuchi et al. Impaired memory in assays of contextual fear conditioning Lasagna-Reeves Neuron loss and brain atrophy by eight to 12 months, especially in the hippocampus and spreading to the neocortex and entorhinal cortex.
Neurofibrillary tangles in the neocortex, amygdala, hippocampus, brain stem, and spinal cord. Neuroinflammation with microgliosis and astrocytosis. Impairments in spatial memory and learning ability in Morris water maze. Paralysis at seven to 10 months associated with a hunched-back posture followed by feeding difficulties. About 80 percent mortality by 12 months with median survival of about nine months. Rare amyloid plaques at 4 months, plaques become more abundant with age.
By 8 months the number of amyloid plaques increases considerably in the subiculum and the CA1 region of the hippocampus Grueninger et al. Abnormally phosphorylated tau is detectable at 4 months in both TauPS2APP and tau single transgenic mice especially in the subiculum, amygdala, and the CA1 region of the hippocampus.
Tau pathology increases with age with numerous tangle-like deposits in the hippocampus confirmed by Gallyas silver staining at 16 months Grueninger et al. Impairment is not age-associated and does not progress from age 4 months to 12 months Grueninger et al. Phosphorylated tau accumulation in the subiculum and the CA1 region of the hippocampus at 4 months.
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Neurofibrillary tangles in these regions as well as the amygdala. Amyloid plaques. Dystrophic neurites and neuropil threads containing abnormally phosphorylated tau. Impaired spatial learning in the Morris water maze at 4 months but impairment is not progressive between 4 and 12 months and appears to be independent of pathology. Congophilic tau inclusions in a subset of forebrain neurons around 18 months of age. Detected by Congo red, thioflavin S, and Gallyas silver stain. Impairments in the contextual and cued fear conditioning test at 16—23 months compared with wild-type littermates.
No detectable sensorimotor deficits. Argyrophilic and congophilic tau inclusions in neurons of the forebrain with age. Detectable with Congo red, thioflavin-S and Gallyas silver stain. Congophilic tau inclusions also in the hippocampus and amygdala. Mainly straight tau filaments. Impairments in contextual and cued fear conditioning at 16—23 months compared with wild-type littermates. Tau tangles and aggregates with as little as months of transgene expression. Tangles start in the entorhinal cortex and amygdala and spread to the neocortex by 15 months. Heterogeneous tangle morphology, including flame-shaped.
Neuronal loss in the dentate gyrus granule neurons following 5 months of transgene expression. Shrinkage of the molecular layer of the hippocampus.
Astrogliosis in the hilus region of the hippocampus after 21 months of transgene expression. Additional increases in GFAP-positive astrocytes in the entorhinal and piriform cortices. Hippocampal synaptic loss as indicated by multiple measures following 9. Reduced synaptophysin immunoreactivity and reduced number of spine synapses as measured by electron microscopy.
Functional changes are associated with structural synaptic changes, local calcium dysregulation, and a decrease in the synaptic vesicle pool. Learning and memory impairments are apparent after 10 months of transgene expression as assessed by the Morris water maze and passive avoidance tasks.
Tau aggregates and tangles as early as months after gene expression. Gallyas silver-positive neurons abundant in the entorhinal cortex and amygdala, spreading to the neocortex by 15 months. Synaptic structural changes and reduced synaptic number. Hippocampal neuronal loss. Reversible learning and memory deficits in the Morris water maze and passive avoidance test. No significant motor deficit, although slight reduction in Rotarod performance.
Fibrillar staining in the hippocampus of 11 month old animals by Congo red birefringence. Absent in 4 month old mice, indicating the formation of these neurofilament-like structures occurs between 4 and 11 months Tanemura et al. Evidence of hippocampal neuronal degeneration in 10 month old animals: As characteristics of apoptosis were not observed, the neurons were thought to be undergoing non-apoptotic atrophic degeneration Tanemura et al.
In hippocampal slices there was an attenuation of the amplitude of Schaffer collateral evoked hippocampal depolarization Tanemura et al. Behavioral abnormalities measured in 11 month-old mice. They spent more time in the open arms of the elevated plus maze and had greater overall locomoter activity. No differences in the Morris water maze compared with non-transgenic mice, suggesting the transgenic animals retain spatial recognition abilities Tanemura et al. SDS-insoluble tau aggregates in hippocampus. Higher overall spontaneous locomotion than non-transgenic littermates in elevated plus maze.
No differences in the Morris water maze. Age-dependent neuronal loss in the CA1 region of the hippocampus. Age-dependent deficits in working and spatial reference memory at 12 months, but not at 3 and 6 months. Marked gliosis in the hippocampus by 12 months. Age-dependent behavioral deficits, including working memory as assessed by the cross maze at 12 months, but not at 3 or 6 months.
Early and persistent decrease in anxiety in the elevated plus maze. Comparable to wild-type in general motor coordination at 3 and 6 months as indicated by the balance-beam test, but impairment at 12 months. Increase in microglial density and size in plaque-forming areas of the brain including the hippocampus, frontal cortex, entorhinal cortex, and occipital cortex in month old hemizygotes Frautschy et al.
By 5 months, there was a decline in LTP in the dentate gyrus after perforant path stimulation compared to wild-type; impairment was not observed at 2 months Jacobsen et al. Differences have been observed between the Schaffer collateral and mossy fiber pathways Jung et al. Oxidative lipid damage, astrogliosis and microgliosis. Plaques develop gradually with age. No plaques at 5 months. Very few small plaques at 6 and 7 months. By 9 months plaques scattered throughout the cortex, hippocampus and amygdala, continue to increase at 12 months.
Similar distribution as Tg Neurofibrillary tangles in the spinal cord and pons as early as 3 months, but more consistent and numerous by 6 months. Tangles morphologically similar to those in JNPL3 mice but older bigenic female mice had a marked increase in neurofibrillary tangles in limbic areas by 6 months, especially the olfactory cortex, entorhinal cortex and amygdala Lewis et al. Increased astrocytosis with age especially in limbic areas with the most neurofibrillary tangles.
Microglia especially concentrated around plaques at 9 and 12 months Lewis et al. Gradual appearance of plaques; by 9 months plaques are scattered throughout the cortex, hippocampus, and amygdala similar to Tg Tau pathology more extensive than JNPL3. Astrocytosis and microgliosis. Motor disturbances similar to JNPL3, with identical range in age of onset. Reduced vocalization and decreased grooming. Age- and dose-dependent neuronal loss in the hippocampus CA1 region of hemizygous and homozygous mice.
No difference at 3 months. Altered synaptophysin staining in the CA3 region of the hippocampus. More pronounced in homozygous mice than hemizygous mice at 8 months. Spatial reference memory is impaired as assessed by Morris water maze at 8 months in homozygous mice and 12 months in hemizygous mice. Deficit is age-dependent and is not detected at 3 months. Impaired contextual fear conditioning at 12 months. Age- and dose-dependent hippocampal neuronal loss is seen in the CA1 region as well as microgliosis and astrogliosis.
Age-dependent spatial learning deficit as demonstrated in the Morris water maze, specifically, the absence of a preference for the target quadrant starting at eight months in homozygous mice and at 12 months in hemizygous mice. Impaired contextual fear conditioning. Plaques are detectable at approximately 12 months and are heterogeneous in morphological structure and size, as well as in terms of fluorescence emitted when stained with luminescent polymers conformational amyloid ligands Philipsson et al.
Microgliosis and astrogliosis are most prominent in the hippocampus, but also found locally around deposits in the cerebral cortex and in thalamus at approximately 12 months Philipsson et al. Extracellular pathology, both cerebrovascular amyloid angiopathy CAA and congophilic parenchymal plaques, mainly found in the cerebral cortex, hippocampus and thalamus. Extracellular amyloid plaque deposition starts at around months of age Lord et al.
Microgliosis and astrogliosis most prominent in the hippocampus, but also locally around deposits in the cerebral cortex and thalamus. Transgene-dependent spatial learning impairment in the Morris water maze months Lord et al. Extracellular amyloid plaque at months, most consistent in the cerebral cortex, hippocampus, and thalamus.
Congophilic parenchymal plaques are predominant, but some mice show marked CAA, particularly in the thalamus. Mild spatial learning deficits at months in Morris water maze and impaired functioning in a passive avoidance test at 16 months. Amyloid deposition progresses with age.
Thioflavin S-positive amyloid deposits at 3 months; dense cored plaques and neuritic pathology by 5 months. Plaques appear first in the subiculum, amygdala and frontal cortex, spread to the dentate gyrus, the olfactory bulb, and later thalamus, cerebral vasculature, and striatum, followed by the cerebellum and brain stem Chishti et al. Variable cell loss by region. No difference in overall cell count, but fewer hippocampal neurons at 6 months Brautigam et al. Reduced synaptophysin immunoreactivity in the vicinity of plaques at 6 months Adalbert et al. Early impairment in acquisition and learning reversal in the reference memory version of the Morris water maze, present by 3 months Chishti et al.
Neurofibrillary tangles are absent Chishti et al. Tau is hyperphosphorylated, nitrosylated and aggregated at months especially in the neocortex, dentate gyrus, and the CA1 and CA3 areas of the hippocampus Bellucci et al. Rapid, early plaque development, with thioflavin S-positive amyloid deposits at 3 months; dense cored plaques and neuritic pathology by 5 months.
Plaques become more extensive with age. Dystrophic neurites at 5 months. Early impairment in acquisition and learning reversal in the reference memory version of the Morris water maze by 3 months. Similar to wild-type in motility, exploratory activity, or neuromuscular function at 7 months as evaluated by the rotarod, hole board and grip strength tests. Age-dependent accumulation of amyloid plaques in hippocampus and cortex between 6 and 26 months of age. Structures similar in appearance to neurofibrillary tangles revealed by Gallyas staining and immunostaining using an antibody directed against phospo-tau.
Amyloid plaques, microgliosis, and astrogliosis by 6 months. Neurofibrillary tangle-like structures at 16 months. Approximate 40 percent loss of neurons in hippocampus and cortex by 16 months. Earliest reported deficits are in reversal learning in the Morris water maze, apparent by 6 months. Pronounced increase in the number of GFAP-positive astrocytes and activated microglia with age months especially in the thalamus and subiculum and to a lesser extent in the cortex Miao et al.
Impaired learning and memory in the Barnes maze task at 3, 9, and 12 months; beginning at 3 months took longer to find the escape hole. No difference in mobility, strength or coordination Xu et al. Diffuse plaque-like deposits around 3 months in the subiculum, hippocampus and cortex. Impaired learning and memory in the Barnes maze task at 3, 9, and 12 months. Beginning at 3 months transgenic mice took longer to find the escape hole. No difference in mobility, strength or coordination. Heterozygous animals develop tau pathology starting at months.
Pathology becomes more severe and widespread with age. Also, a significant reduction in the number of choline acetyltransferase ChAT -immunopositive cholinergic neurons in the medial septum has been reported Belarbi et al. Altered paired pulse facilitation PPF , a form of presynaptic short-term plasticity in month old heterozygous animals: PPF increased at 10 ms. Also at this age, impaired maintenance of long term depression as compared with wild-type littermates Van der Jeugd et al.
Deficit in basal synaptic transmission in the hippocampus, but normal LTP Schindowski et al. Non-spatial memory affected as early as 6 months; spatial memory impaired only after 9 months Van der Jeugd et al. Impaired appetitive responding Lo et al. A variety of tau pathologies starting at 3 months, including neurofibrillary tangle-like inclusions, rare ghost tangles, and paired helical filament-like structures.
Hyperphosphorylation of tau on many epitopes e. Increased anxiety and delayed learning from 3 months, and reduced spatial memory at 10 months. No changes in overall motor activity and no gross motor deficits. Increased depression-like and aggressive behavior, co-occurring with disturbances in nocturnal activity. Increased total tau, and phosphorylated tau Thr, Ser, Thr in amygdala and hippocampus starting at 3 months.
Spatial memory deficits starting at 5 months Morris water maze.
Olfactory deficits at 5 months Buried food test. No motor deficits rota rod, beam walk or depressive behavior forced swim test. Microgliosis observed; however, fewer plaque-associated microglia and altered microglial morphology more ramified processes compared with 5xFAD at 7 months, the only age examined. Amyloid plaques with plaque-associated microgliosis.
Reduced plaque burden, altered microglial and plaque morphology, and less severe plaque-associated neuritic dystrophy, compared with 5xFAD. Microgliosis observed in 8. Fewer plaque-associated microglia in mice expressing the R47H variant, compared with the common variant of human TREM2. X Tangles at 52 By 12 months extensive tau immunoreactivity in CA1 neurons of the hippocampus, particularly pyramidal neurons, later in the cortex. No Data Neuronal Loss at Unknown.
Transgenic; PSEN1: Transgenic; MAPT: X Neuronal Loss at 39 Neuron loss in cortical layer 5 and subiculum. X Gliosis at 9 Gliosis begins at 2 months Oakley et al. X Synaptic Loss at 39 Synaptic markers synaptophysin, syntaxin, and PSD decrease with age and are significantly reduced by 9 and 12 months. X Cognitive Impairment at 17 Impaired spatial memory in Y-maze test at months. Absent Tangles at Absent. No Data. Transgenic Alzheimer's Disease Amyloid pathology starting at 2 months, including amyloid plaques.
No Data Tangles at No data. Neuronal Loss at No data. Gliosis at No data. Synaptic Loss at No data. Cognitive Impairment at No data. Transgenic Alzheimer's Disease Progressive amyloid deposition in the cerebral cortex by approximately months. No Data Plaques at No data. Tangles at No data. Knock-In; Trem2: Knock-In Alzheimer's Disease Unknown. ADanPP Observed X Plaques at 9 Vascular amyloid deposits and punctate parenchymal aggregates first occur in the hippocampus and increase with age, spreading throughout the brain, including the cortex, amygdala, thalamus, and brainstem in hemizygous mice.
X Gliosis at 17 Astrogliosis and microgliosis increase with age and increasing ADan-amyloid deposition. X Cognitive Impairment at 78 The only ages tested were 6 months and months. Neuronal Loss at Absent. No Data Synaptic Loss at Unknown. Transgenic Familial Danish Dementia, Alzheimer's Disease, Cerebral Amyloid Angiopathy ADan deposition starts in the hippocampus and meningeal vessels at 2 months and increases with age. Knock-In Alzheimer's Disease No data. No data. X Cognitive Impairment at 12 Male rats show deficits in Morris water maze as early as 3 months of age. Absent Plaques at Do not spontaneously develop amyloid pathology, but can serve as hosts for exogenously seeded amyloid deposits.
Transgenic Alzheimer's Disease No plaques to 30 months of age. APP23 Observed X Plaques at 26 Congophillic, dense-core amyloid plaques first appear at 6 months, and increase in size and number with age. X Gliosis at 26 Activated microglia in close proximity to dense amyloid plaques Stalder et al. X Cognitive Impairment at 13 Spatial memory defects in Morris Water maze at 3 months and progresses with age Van dam et al. Synaptic Loss at Neocortical synapses were examined in mice as old as 24 months of age; no evidence of alterations in the number of synapses or levels of synaptophysin were observed Boncristiano et al.
X Gliosis at 39 Astrocytosis in the vicinity of plaques in the hippocampus and cortex by 9 months. X Cognitive Impairment at 13 Short-term memory deficits are apparent by 3 to 4 months as measured by the Y maze. Absent Tangles at Not observed. No Data Neuronal Loss at No data. Knock-In Alzheimer's Disease Amyloid deposition by 6 months of age in the cortex and hippocampus. Short-term memory deficits apparent by months as measured by the Y maze. X Neuronal Loss at 23 Some cell loss detectable as early as 6 months in female mice. X Synaptic Loss at 24 At 6 months, levels of pre- and post-synaptic markers are reduced Breyhan et al.
X Cognitive Impairment at 27 Age-dependent impairments in working memory as measured by the Y maze and T-maze continuous alternation task. Tangles at Absent. Synaptic Loss at Unknown. Cognitive Impairment at Unknown. X Gliosis at 52 At 12 months of age, microgliosis is seen in transgenic mice, as measured by the presence of Iba-1 staining in the hippocampus and cortex.
X Synaptic Loss at 34 Starting around eight months of age, transgenic mice exhibit a decrease in synaptic density in the CA3 region of the hippocampus as measured by synaptophysin staining. X Cognitive Impairment at 36 By 8 months of age, transgenic mice exhibit memory impairment in the Morris water maze compared to mice expressing equivalent levels of wild-type human APP. Tangles at Overt tangle pathology is not observed out to 24 months of age, but abnormal tau phosphorylation is observed starting around eight months of age.
Knock-In; App: Knock-Out; Trem2: X Gliosis at 26 Microglia and activated astrocytes accumulate with age, starting around 6 months of age, concurrent with plaque formation. X Cognitive Impairment at 78 Memory impairment in homozygous mice at 18 months as measured by the Y maze test. Absent Tangles at Absent; although elevated levels of phosphorylated tau are observed in dystrophic neurites around plaques. X Gliosis at 9 Microglia and activated astrocytes accumulate with age starting around 2 months, especially around plaques in a manner concurrent with plaque formation.
X Cognitive Impairment at 26 Memory impairment in homozygous mice by 6 months of age as measured by the Y maze.
Absent Tangles at Absent; although phosphorylated tau is elevated in dystrophic neurites around plaques. Knock-In Alzheimer's Disease Aggressive amyloidosis with deposition in the cortex beginning at 2 months and approaching saturation by 7 months. Memory impairment by 6 months as measured by the Y maze. X Neuronal Loss at 74 Global neuron loss is not observed, but modest neuron loss was found in the granule cell layer of the dentate gyrus and other subregions with high neuronal density in month old animals Rupp et al. X Synaptic Loss at 10 Dendritic spine loss around plaques reported to begin approximately 4 weeks after plaque formation and continue for several months Bittner et al.
X Cognitive Impairment at 30 Cognitive deficits in spatial learning and memory in the Morris water maze reported at 7 months Serneels et al. Absent Tangles at Phosphorylated tau-positive neuritic processes around plaques have been observed, but no mature tangles Radde et al. Transgenic Alzheimer's Disease Amyloid plaque deposition starts at approximately 6 weeks in the neocortex. X Neuronal Loss at 76 Necrotic neurons in hippocampus and cortex. X Cognitive Impairment at 40 Deficits in Barnes maze at 10 months.
Transgenic Alzheimer's Disease Amyloid plaques, cerebral amyloid angiopathy, and necrotic neurons in hippocampus and cortex by 19 months of age. Deficits in Barnes maze by 10 months of age. X Neuronal Loss at 36 Neuronal loss observed adjacent to plaques relative to more distal areas. X Gliosis at 37 Increased astrocytosis adjacent to plaques relative to more distal areas. X Synaptic Loss at 40 Decreased synapse density adjacent to plaques relative to more distal areas. Absent Tangles at No tangles. Aggregates of misfolded and phosphorylated tau observed between months.
Knock-In Alzheimer's Disease Tau accumulations, dystrophic neurites, astrocytosis, neuronal loss, and synapse loss were more pronounced adjacent to cortical plaques. Strategy Security: Mobigame S. Zombie Tsunami Android Game Attack the city with zombies!
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