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Myo-inositol changes precede amyloid pathology and relate to APOE genotype in Alzheimer disease.

Voevodskaya O, Sundgren PC, Strandberg O, Zetterberg H, Minthon L, Blennow K, Wahlund LO, Westman E, Hansson O, Swedish BioFINDER study gro - Neurology (2016)

Bottom Line: Amyloid-positive cognitively healthy participants showed a significant increase in mI/creatine and mI/NAA levels compared to amyloid-negative healthy elderly (p < 0.05).In amyloid-positive healthy elderly, mI/creatine and mI/NAA correlated with cortical retention of [(18)F] flutemetamol tracer ([Formula: see text] = 0.44, p = 0.02 and [Formula: see text] = 0.51, p = 0.01, respectively).Healthy elderly APOE ε4 carriers with normal CSF Aβ42 levels had significantly higher mI/creatine levels (p < 0.001) than ε4 noncarriers.

View Article: PubMed Central - PubMed

Affiliation: From Clinical Geriatrics (O.V., L.-O.W., E.W.), Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Stockholm; Department of Diagnostic Radiology (P.C.S., O.S.), Lund University; Clinical Neurochemistry Laboratory (H.Z., K.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; UCL Institute of Neurology (H.Z.), Queen Square, London, UK; Memory Clinic (L.M., O.H.), Skåne University Hospital; and Clinical Memory Research Unit (L.M., O.H.), Department of Clinical Sciences, Malmö, Lund University, Sweden. olga.voevodskaya@ki.se oskar.hansson@med.lu.se.

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Related in: MedlinePlus

Concentrations of myo-inositol (mI)/creatine (Cr) in posterior cingulate cortex/precuneus in the diagnostic subgroups stratified by APOE ε4 carriershipLevels of mI/Cr differed significantly between carriers and noncarriers in the subgroup of CSF Aβ42-negative controls (t = −3.61, p < 0.001). CTL Aβ42− = controls with CSF Aβ42 >530 ng/L; CTL Aβ42+ = controls with CSF Aβ42 ≤530 ng/L; SCD Aβ42+ = patients with subjective cognitive decline with CSF Aβ42 ≤530 ng/L; MCI Aβ42+ = patients with mild cognitive impairment with CSF Aβ42 ≤530 ng/L.
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Figure 3: Concentrations of myo-inositol (mI)/creatine (Cr) in posterior cingulate cortex/precuneus in the diagnostic subgroups stratified by APOE ε4 carriershipLevels of mI/Cr differed significantly between carriers and noncarriers in the subgroup of CSF Aβ42-negative controls (t = −3.61, p < 0.001). CTL Aβ42− = controls with CSF Aβ42 >530 ng/L; CTL Aβ42+ = controls with CSF Aβ42 ≤530 ng/L; SCD Aβ42+ = patients with subjective cognitive decline with CSF Aβ42 ≤530 ng/L; MCI Aβ42+ = patients with mild cognitive impairment with CSF Aβ42 ≤530 ng/L.

Mentions: Finally, we aimed to study the relationship between APOE and MRS metabolites in different stages of predementia AD. GLM analysis revealed that healthy APOE ε4 carriers with still normal CSF Aβ42 levels had significantly higher mI/Cr concentrations than APOE ε4 noncarriers (t = −3.61, d = 0.47, p < 0.001). APOE ε4 carriership did not influence mI/Cr levels in the remaining diagnostic groups—those where CSF Aβ42 levels were already abnormal (figure 3).


Myo-inositol changes precede amyloid pathology and relate to APOE genotype in Alzheimer disease.

Voevodskaya O, Sundgren PC, Strandberg O, Zetterberg H, Minthon L, Blennow K, Wahlund LO, Westman E, Hansson O, Swedish BioFINDER study gro - Neurology (2016)

Concentrations of myo-inositol (mI)/creatine (Cr) in posterior cingulate cortex/precuneus in the diagnostic subgroups stratified by APOE ε4 carriershipLevels of mI/Cr differed significantly between carriers and noncarriers in the subgroup of CSF Aβ42-negative controls (t = −3.61, p < 0.001). CTL Aβ42− = controls with CSF Aβ42 >530 ng/L; CTL Aβ42+ = controls with CSF Aβ42 ≤530 ng/L; SCD Aβ42+ = patients with subjective cognitive decline with CSF Aβ42 ≤530 ng/L; MCI Aβ42+ = patients with mild cognitive impairment with CSF Aβ42 ≤530 ng/L.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4862247&req=5

Figure 3: Concentrations of myo-inositol (mI)/creatine (Cr) in posterior cingulate cortex/precuneus in the diagnostic subgroups stratified by APOE ε4 carriershipLevels of mI/Cr differed significantly between carriers and noncarriers in the subgroup of CSF Aβ42-negative controls (t = −3.61, p < 0.001). CTL Aβ42− = controls with CSF Aβ42 >530 ng/L; CTL Aβ42+ = controls with CSF Aβ42 ≤530 ng/L; SCD Aβ42+ = patients with subjective cognitive decline with CSF Aβ42 ≤530 ng/L; MCI Aβ42+ = patients with mild cognitive impairment with CSF Aβ42 ≤530 ng/L.
Mentions: Finally, we aimed to study the relationship between APOE and MRS metabolites in different stages of predementia AD. GLM analysis revealed that healthy APOE ε4 carriers with still normal CSF Aβ42 levels had significantly higher mI/Cr concentrations than APOE ε4 noncarriers (t = −3.61, d = 0.47, p < 0.001). APOE ε4 carriership did not influence mI/Cr levels in the remaining diagnostic groups—those where CSF Aβ42 levels were already abnormal (figure 3).

Bottom Line: Amyloid-positive cognitively healthy participants showed a significant increase in mI/creatine and mI/NAA levels compared to amyloid-negative healthy elderly (p < 0.05).In amyloid-positive healthy elderly, mI/creatine and mI/NAA correlated with cortical retention of [(18)F] flutemetamol tracer ([Formula: see text] = 0.44, p = 0.02 and [Formula: see text] = 0.51, p = 0.01, respectively).Healthy elderly APOE ε4 carriers with normal CSF Aβ42 levels had significantly higher mI/creatine levels (p < 0.001) than ε4 noncarriers.

View Article: PubMed Central - PubMed

Affiliation: From Clinical Geriatrics (O.V., L.-O.W., E.W.), Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Stockholm; Department of Diagnostic Radiology (P.C.S., O.S.), Lund University; Clinical Neurochemistry Laboratory (H.Z., K.B.), Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; UCL Institute of Neurology (H.Z.), Queen Square, London, UK; Memory Clinic (L.M., O.H.), Skåne University Hospital; and Clinical Memory Research Unit (L.M., O.H.), Department of Clinical Sciences, Malmö, Lund University, Sweden. olga.voevodskaya@ki.se oskar.hansson@med.lu.se.

No MeSH data available.


Related in: MedlinePlus