• significant decrease in amyloid beta senile plaques compared to transgenic mice wild-type for Gsk3a

• performance in a Barnes maze and in an open field are similar to wild-type controls unlike transgenic mice wild-type for Gsk3a (J:184975)

• significant decrease in amyloid beta senile plaques compared to transgenic mice wild-type for Gsk3a

• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex

• deposits are diffuse in appearance; deposition is prominent in dentate hilus, but little or none in molecular layer of dentate gyrus

• at 12 months, mice have high levels of insoluble Abeta₄₂

• at 3 months, cerebral spinal fluid levels of Abeta₄₀ and Abeta₄₂ are elevated; Abeta₄₀ increase is greater than in transgenic, Apoe-single null animals

• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex

• deposits are diffuse in appearance; deposition is prominent in dentate hilus, but little or none in molecular layer of dentate gyrus

• at 12 months, mice have high levels of insoluble Abeta₄₂

• at 3 months, cerebral spinal fluid levels of Abeta₄₀ and Abeta₄₂ are elevated; Abeta₄₀ increase is greater than in transgenic, Apoe-single null animals

• at 6 months of age, most mice have substantial amyloid beta (Abeta) deposits

• by 12 months of age, mice have more amyloid beta (Abeta) deposits in the hippocampus and cortex than other genotypes

• Abeta deposits are more numerous and fill all parts of hippocampus and some of the cortex by 12 months; abundant compact and diffuse plaques are observed

• mice have greater levels of thioflavine-S-positive (fibrillar) Abeta deposits than other genotypes, similar to transgenic homozygotes with normal Apoe and Clu

• at 3 months, cerebral spinal fluid levels of Abeta₄₀ and Abeta₄₂ are elevated

• mice have significant amyloid burden, greater than shown by other genotypes

• at 12 months, mice have highest tissue levels of soluble Abeta₄₀ and Abeta₄₂, with high levels of insoluble Abeta₄₂

• at 3 months, mice have higher levels of carbonate soluble Abeta₄₀ and Abeta₄₂ compared to other genotypes

• at 6 months of age, most mice have substantial amyloid beta (Abeta) deposits

• by 12 months of age, mice have more amyloid beta (Abeta) deposits in the hippocampus and cortex than other genotypes

• Abeta deposits are more numerous and fill all parts of hippocampus and some of the cortex by 12 months; abundant compact and diffuse plaques are observed

• mice have greater levels of thioflavine-S-positive (fibrillar) Abeta deposits than other genotypes, similar to transgenic homozygotes with normal Apoe and Clu

• at 3 months, cerebral spinal fluid levels of Abeta₄₀ and Abeta₄₂ are elevated

• 40% of mice exhibit plaque depositions at 12 months of age with one mouse remaining plaque free at 21 months (J:127846)

• 23% of mice at 15 months, 33% at 18 months and 55% at 21 months exhibit fibrillar plaques in the outer molecular layer of the dentate gyrus (J:127846)

• mice exhibit plaques in the stratum oriens and radiatum of the hippocampus and hilus of the dentate gyrus (J:127846)

• 3 of 4 mice exhibit plaques by 12 months of age (J:133058)

• 40% of mice exhibit plaque depositions at 12 months of age with one mouse remaining plaque free at 21 months (J:127846)

• 23% of mice at 15 months, 33% at 18 months and 55% at 21 months exhibit fibrillar plaques in the outer molecular layer of the dentate gyrus (J:127846)

• mice exhibit plaques in the stratum oriens and radiatum of the hippocampus and hilus of the dentate gyrus (J:127846)

• 3 of 4 mice exhibit plaques by 12 months of age (J:133058)

• by 15 to 18 months, 60% of mice exhibit plaques in the hippocampus (J:127846)

• the amount of amyloid deposited is more than in Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoe^tm1Unc/Apoe^tm1Unc mice but much less than in Tg(APPV717F)109Ili Apoe^tm1Unc/Apoe^tm1Unc mice (J:127846)

• plaques are observed in the outer molecular layer of the dentate gyrus and the stratum oriens and radiatum of the hippocampus (J:127846)

• mice exhibit fibrillar plaques in the outer molecular layer of the dentate gyrus (J:127846)

• 55.6% of mice exposed to traumatic brain injury (TBI) at 9 to 10 months of age exhibit amyloid plaques by 12 to 13 months of age while mice not exposed to TBI do not exhibit plaques until 15 months of age (J:133058)

• mice exhibit increased plaque formation and severity following TBI compared to in similarly treated Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoe^tm1Unc/Apoe^tm1Unc mice (J:133058)

• 44% of mice exhibit thioflavine-S+ amyloid staining (fibrillar amyloid) in the molecular layer unlike in Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoe^tm1Unc/Apoe^tm1Unc and Tg(APPV717F)109Ili Apoe^tm1Unc/Apoe^tm1Unc mice (J:133058)

• by 15 to 18 months, 60% of mice exhibit plaques in the hippocampus (J:127846)

• the amount of amyloid deposited is more than in Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoe^tm1Unc/Apoe^tm1Unc mice but much less than in Tg(APPV717F)109Ili Apoe^tm1Unc/Apoe^tm1Unc mice (J:127846)

• plaques are observed in the outer molecular layer of the dentate gyrus and the stratum oriens and radiatum of the hippocampus (J:127846)

• mice exhibit fibrillar plaques in the outer molecular layer of the dentate gyrus (J:127846)

• 55.6% of mice exposed to traumatic brain injury (TBI) at 9 to 10 months of age exhibit amyloid plaques by 12 to 13 months of age while mice not exposed to TBI do not exhibit plaques until 15 months of age (J:133058)

• mice exhibit increased plaque formation and severity following TBI compared to in similarly treated Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoe^tm1Unc/Apoe^tm1Unc mice (J:133058)

• 44% of mice exhibit thioflavine-S+ amyloid staining (fibrillar amyloid) in the molecular layer unlike in Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoe^tm1Unc/Apoe^tm1Unc and Tg(APPV717F)109Ili Apoe^tm1Unc/Apoe^tm1Unc mice (J:133058)

• by 15 to 18 months, 31% of mice exhibit plaques in the hippocampus (J:127846)

• the amount of amyloid deposited is less than in Tg(APPV717F)109Ili Tg(GFAP-APOE_i4)#Hol Apoe^tm1Unc/Apoe^tm1Unc and much less than in Tg(APPV717F)109Ili Apoe^tm1Unc/Apoe^tm1Unc mice (J:127846)

• plaques are observed in the the outer molecular layer of the dentate gyrus and the stratum oriens and radiatum of the hippocampus (J:127846)

• mice exhibit fibrillar plaques in the outer molecular layer of the dentate gurys (J:127846)

• 20% of mice exposed to traumatic brain injury (TBI) at 9 to 10 months of age exhibit amyloid plaques by 12 to 13 months of age while mice not exposed to TBI do not exhibit plaques until 15 months of age (J:133058)

• mice exhibit decreased plaque formation and severity following TBI compared to in similarly treated Tg(APPV717F)109Ili Tg(GFAP-APOE_i4)#Hol Apoe^tm1Unc/Apoe^tm1Unc mice (J:133058)

• by 15 to 18 months, 31% of mice exhibit plaques in the hippocampus (J:127846)

• the amount of amyloid deposited is less than in Tg(APPV717F)109Ili Tg(GFAP-APOE_i4)#Hol Apoe^tm1Unc/Apoe^tm1Unc and much less than in Tg(APPV717F)109Ili Apoe^tm1Unc/Apoe^tm1Unc mice (J:127846)

• plaques are observed in the the outer molecular layer of the dentate gyrus and the stratum oriens and radiatum of the hippocampus (J:127846)

• mice exhibit fibrillar plaques in the outer molecular layer of the dentate gurys (J:127846)

• 20% of mice exposed to traumatic brain injury (TBI) at 9 to 10 months of age exhibit amyloid plaques by 12 to 13 months of age while mice not exposed to TBI do not exhibit plaques until 15 months of age (J:133058)

• mice exhibit decreased plaque formation and severity following TBI compared to in similarly treated Tg(APPV717F)109Ili Tg(GFAP-APOE_i4)#Hol Apoe^tm1Unc/Apoe^tm1Unc mice (J:133058)

• 66% of mice exhibit plaques after 18 months

• mice exhibit plaques in the stratum oriens and radiatum of the hippocampus and hilus of the dentate gyrus but no the molecular layer of the dentate gyrus

• however, no fibrillar plaques are detected

• 66% of mice exhibit plaques after 18 months

• mice exhibit plaques in the stratum oriens and radiatum of the hippocampus and hilus of the dentate gyrus but no the molecular layer of the dentate gyrus

• however, no fibrillar plaques are detected

• a 10-fold reduction in dystrophic neurites in hippocampi at 12 months compared to Clu-sufficient transgenic mice and a 5-fold reduction in number of dystrophic neurites per amyloid deposit

• by 12 months of age, ~60% of mice show amyloid beta (Abeta) deposition (J:78357)

• decreased percentage of Abeta-immunoreactive deposits that are thioflavine-S-positive (2.46 vs 19.4% thioflavine load/Abeta load) compared to Clu-sufficient mice (J:78357)

• many Abeta deposits have few or no detectable dystrophic neurites around them (J:78357)

• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex (J:107702)

• only 20% of mice have thioflavine-S-positive (fibrillar Abeta or amyloid) deposits in the cortex at 12 months

• mice have lower hippocampal amyloid burden (0.89%) at 12 months than Clu-sufficient transgenic mice; amyloid load increases to 2.25% by 15 months

• by 12 months of age, ~60% of mice show amyloid beta (Abeta) deposition (J:78357)

• decreased percentage of Abeta-immunoreactive deposits that are thioflavine-S-positive (2.46 vs 19.4% thioflavine load/Abeta load) compared to Clu-sufficient mice (J:78357)

• many Abeta deposits have few or no detectable dystrophic neurites around them (J:78357)

• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex (J:107702)

• develop reactive astrocytosis

• elevated amyloid deposits over controls

• elevated amyloid deposits over controls

• loss of synaptophysin-immunoreactive presynaptic terminals in the hippocampal outer molecular layer (loss was similar to that seen in wild-type (Msr1+) mice heterozygous for Tg(APP)109Ili )

• reduced density of MAP-2 immuoreactive neuronal dendrites in the outer molecular layer of the hippocampus (loss was similar to that seen in wild-type (Msr1+) mice heterozygous for Tg(APP)109Ili)

• number and distribution of plaques was similar to those seen in wild-type (Msr1+) mice heterozygous for Tg(APP)109Ili

• number and distribution of plaques was similar to those seen in wild-type (Msr1+) mice heterozygous for Tg(APP)109Ili

• at 12 months, rare amyloid beta (Abeta) deposits are observed in the cortex, with occasional deposits in the molecular layer of hippocampus and frequent Abeta deposits in the hilus of the dentate gyrus; mice show 3-fold less Abeta in the brain relative to Tg(APPV717F)109Ili, Abca1-wild-type controls

• fibrillar Abeta plaques are frequently observed in cortex and hippocampus

• Abeta deposits are almost all diffuse, with little true amyloid

• very few clusters of reactive microglia are seen in brain

• at 12 months, rare amyloid beta (Abeta) deposits are observed in the cortex, with occasional deposits in the molecular layer of hippocampus and frequent Abeta deposits in the hilus of the dentate gyrus; mice show 3-fold less Abeta in the brain relative to Tg(APPV717F)109Ili, Abca1-wild-type controls

• fibrillar Abeta plaques are frequently observed in cortex and hippocampus

• Abeta deposits are almost all diffuse, with little true amyloid

• very few clusters of reactive microglia are seen in brain

• dystrophic neurites are 10-fold higher compared to Clu-null transgenic mice and more dystrophic neurites (5-fold) are associated with each amyloid deposit

• by 12 months of age, ~60% of mice show amyloid beta (Abeta) deposition (J:78357)

• mice have a higher percentage of thioflavine-S positive Abeta-immunoreactive deposits than Clu-null mice (J:78357)

• all deposits are surrounded by multiple enlarged, dystrophic neurites (J:78357)

• a 2-fold increase in monomeric Abeta is detected in the brain compared to Clu-deficient transgenic mice (J:78357)

• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex (J:107702)

• mice have prominent deposits that are both diffuse and compact in appearance in hippocampus and in molecular layer of dentate gyrus (J:107702)

• 77% of mice have thioflavine-S-positive (fibrillar Abeta or amyloid) deposits in the cortex

• hippocampal amyloid burden is greater (2.76%) than in Clu-null transgenics at 12 months of age

• by 12 months of age, ~60% of mice show amyloid beta (Abeta) deposition (J:78357)

• mice have a higher percentage of thioflavine-S positive Abeta-immunoreactive deposits than Clu-null mice (J:78357)

• all deposits are surrounded by multiple enlarged, dystrophic neurites (J:78357)

• a 2-fold increase in monomeric Abeta is detected in the brain compared to Clu-deficient transgenic mice (J:78357)

• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex (J:107702)

• mice have prominent deposits that are both diffuse and compact in appearance in hippocampus and in molecular layer of dentate gyrus (J:107702)

• significant deficits in latency to find the target on the Barnes maze and use a poor maze strategy

• increase in locomotor activity in an open field

• mice do not show neuronal loss in the hippocampal regions compared to Tg(PDGFB-APP*V717F)H6Lms mice (J:100974)

• synaptic and dendritic density are reduced in the molecular layer

• amyoid plaques are associated with distorted neurites

• the majority of amyloid plaques are surrounded by GFAP-positive reactive astrocytes

• deposits of human beta-amyloid are seen in the hippocampus, corpus callosum and cerebral cortex, beginning at 6 - 9 months, and increasing in density with age (J:23080)

• mice develop plaques by 12 months of age in the hippocampus and the outer molecular layer of the dentate gyrus with a subset of plaques positive for fibrillar amyloid (J:127846)

• plaque deposition increases with age with greater than 85% of the hippocampus covered in plaques at 24 months of age (J:127846)

• deposits of human beta-amyloid are seen in the hippocampus, corpus callosum and cerebral cortex, beginning at 6 - 9 months, and increasing in density with age (J:23080)

• mice develop plaques by 12 months of age in the hippocampus and the outer molecular layer of the dentate gyrus with a subset of plaques positive for fibrillar amyloid (J:127846)

• plaque deposition increases with age with greater than 85% of the hippocampus covered in plaques at 24 months of age (J:127846)