Shapes of the Trajectories of 5 Major Biomarkers of Alzheimer Disease

Deficits in hippocampal‐dependent transfer generalization learning accompany synaptic dysfunction in a mouse model of amyloidosis

“…As described in the current study, both Aβ40 and Aβ42 levels are significantly elevated by this age in APP swe PS1 mice; however Aβ deposition in the hippocampus is not widespread (Holcomb et al, ; Wengenack et al, ; Jankowsky et al, ; Burgess et al, ). These data agree with a growing literature that suggests that soluble β‐amyloid can detrimentally impact neuronal communication and synaptic integrity, even in the absence of extensive plaque deposition (Oddo et al, ; Jack et al, ).…”

Deficits in hippocampal‐dependent transfer generalization learning accompany synaptic dysfunction in a mouse model of amyloidosis

“…As described in the current study, both Aβ40 and Aβ42 levels are significantly elevated by this age in APP swe PS1 mice; however Aβ deposition in the hippocampus is not widespread (Holcomb et al, ; Wengenack et al, ; Jankowsky et al, ; Burgess et al, ). These data agree with a growing literature that suggests that soluble β‐amyloid can detrimentally impact neuronal communication and synaptic integrity, even in the absence of extensive plaque deposition (Oddo et al, ; Jack et al, ).…”

AD-Related CSF Biomarkers Across Distinct Levels of Cognitive Impairment: Correlations With Global Cognitive State

“…Conversely, Spies et al 12 and Tsolaki et al 13 did not find correlations between CAMCOG total scores and levels of any CSF biomarkers. Our results agree with those by Jack et al 39 and Vemuri et al 11 regarding T-tau levels, but we could not find correlations between global cognition and Aβ 42 or p-Tau levels.…”

Cerebrospinal fluid phospho-tau T217 outperforms T181 as a biomarker for the differential diagnosis of Alzheimer’s disease and PET amyloid-positive patient identification

“…The present results also show that the pT217 levels are strongly indicative of the amyloid plaque load, as measured with PiB-PET. This finding is in line with longitudinal studies showing that amyloid impairments are involved in tau pathology [11,[43][44][45][46]. The molecular mechanism whereby amyloid and Tau pathologies contribute to AD might depend on the influence of Aβ on kinases such as GSK-3β [47,48], which might result in the phosphorylation of tau at many sites, including T181 and pT217 [34].…”

Deficits in hippocampal‐dependent transfer generalization learning accompany synaptic dysfunction in a mouse model of amyloidosis

“…As described in the current study, both Aβ40 and Aβ42 levels are significantly elevated by this age in APP swe PS1 mice; however Aβ deposition in the hippocampus is not widespread (Holcomb et al, ; Wengenack et al, ; Jankowsky et al, ; Burgess et al, ). These data agree with a growing literature that suggests that soluble β‐amyloid can detrimentally impact neuronal communication and synaptic integrity, even in the absence of extensive plaque deposition (Oddo et al, ; Jack et al, ).…”

AD-Related CSF Biomarkers Across Distinct Levels of Cognitive Impairment: Correlations With Global Cognitive State

“…Conversely, Spies et al 12 and Tsolaki et al 13 did not find correlations between CAMCOG total scores and levels of any CSF biomarkers. Our results agree with those by Jack et al 39 and Vemuri et al 11 regarding T-tau levels, but we could not find correlations between global cognition and Aβ 42 or p-Tau levels.…”

Cerebrospinal fluid phospho-tau T217 outperforms T181 as a biomarker for the differential diagnosis of Alzheimer’s disease and PET amyloid-positive patient identification

“…The present results also show that the pT217 levels are strongly indicative of the amyloid plaque load, as measured with PiB-PET. This finding is in line with longitudinal studies showing that amyloid impairments are involved in tau pathology [11,[43][44][45][46]. The molecular mechanism whereby amyloid and Tau pathologies contribute to AD might depend on the influence of Aβ on kinases such as GSK-3β [47,48], which might result in the phosphorylation of tau at many sites, including T181 and pT217 [34].…”

Deficits in hippocampal‐dependent transfer generalization learning accompany synaptic dysfunction in a mouse model of amyloidosis

“…As described in the current study, both Aβ40 and Aβ42 levels are significantly elevated by this age in APP swe PS1 mice; however Aβ deposition in the hippocampus is not widespread (Holcomb et al, ; Wengenack et al, ; Jankowsky et al, ; Burgess et al, ). These data agree with a growing literature that suggests that soluble β‐amyloid can detrimentally impact neuronal communication and synaptic integrity, even in the absence of extensive plaque deposition (Oddo et al, ; Jack et al, ).…”

AD-Related CSF Biomarkers Across Distinct Levels of Cognitive Impairment: Correlations With Global Cognitive State

“…Conversely, Spies et al 12 and Tsolaki et al 13 did not find correlations between CAMCOG total scores and levels of any CSF biomarkers. Our results agree with those by Jack et al 39 and Vemuri et al 11 regarding T-tau levels, but we could not find correlations between global cognition and Aβ 42 or p-Tau levels.…”

Cerebrospinal fluid phospho-tau T217 outperforms T181 as a biomarker for the differential diagnosis of Alzheimer’s disease and PET amyloid-positive patient identification

“…The present results also show that the pT217 levels are strongly indicative of the amyloid plaque load, as measured with PiB-PET. This finding is in line with longitudinal studies showing that amyloid impairments are involved in tau pathology [11,[43][44][45][46]. The molecular mechanism whereby amyloid and Tau pathologies contribute to AD might depend on the influence of Aβ on kinases such as GSK-3β [47,48], which might result in the phosphorylation of tau at many sites, including T181 and pT217 [34].…”