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Topics {✒️}

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         headline:Tracking reactive astrogliosis in autosomal dominant and sporadic Alzheimer’s disease with multi-modal PET and plasma GFAP
         description:Plasma assays for the detection of Alzheimer’s disease neuropathological changes are receiving ever increasing interest. The concentration of plasma glial fibrillary acidic protein (GFAP) has been suggested as a potential marker of astrocytes or recently, amyloid-β burden, although this hypothesis remains unproven. We compared plasma GFAP levels with the astrocyte tracer 11C-Deuterium-L-Deprenyl (11C-DED) in a multi-modal PET design in participants with sporadic and Autosomal Dominant Alzheimer’s disease. Twenty-four individuals from families with known Autosomal Dominant Alzheimer’s Disease mutations (mutation carriers = 10; non-carriers = 14) and fifteen patients with sporadic Alzheimer’s disease were included. The individuals underwent PET imaging with 11C-DED, 11C-PIB and 18F-FDG, as markers of reactive astrogliosis, amyloid-β deposition, and glucose metabolism, respectively, and plasma sampling for measuring GFAP concentrations. Twenty-one participants from the Autosomal Dominant Alzheimer’s Disease group underwent follow-up plasma sampling and ten of these participants underwent follow-up PET imaging. In mutation carriers, plasma GFAP levels and 11C-PIB binding increased, while 11C-DED binding and 18F-FDG uptake significantly decreased across the estimated years to symptom onset. Cross-sectionally, plasma GFAP demonstrated a negative correlation with 11C-DED binding in both mutation carriers and patients with sporadic disease. Plasma GFAP indicated cross-sectionally a significant positive correlation with 11C-PIB binding and a significant negative correlation with 18F-FDG in the whole sample. The longitudinal levels of 11C-DED binding showed a significant negative correlation with longitudinal plasma GFAP concentrations over the follow-up interval. Plasma GFAP concentration and astrocyte 11C-DED brain binding levels followed divergent trajectories and may reflect different underlying processes. The strong negative association between plasma GFAP and 11C-DED binding in Autosomal Dominant and sporadic Alzheimer’s disease brains may indicate that if both are markers of reactive astrogliosis, they may detect different states or subtypes of astrogliosis. Increased 11C-DED brain binding seems to be an earlier phenomenon in Alzheimer’s disease progression than increased plasma GFAP concentration.
         datePublished:2023-09-12T00:00:00Z
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      headline:Tracking reactive astrogliosis in autosomal dominant and sporadic Alzheimer’s disease with multi-modal PET and plasma GFAP
      description:Plasma assays for the detection of Alzheimer’s disease neuropathological changes are receiving ever increasing interest. The concentration of plasma glial fibrillary acidic protein (GFAP) has been suggested as a potential marker of astrocytes or recently, amyloid-β burden, although this hypothesis remains unproven. We compared plasma GFAP levels with the astrocyte tracer 11C-Deuterium-L-Deprenyl (11C-DED) in a multi-modal PET design in participants with sporadic and Autosomal Dominant Alzheimer’s disease. Twenty-four individuals from families with known Autosomal Dominant Alzheimer’s Disease mutations (mutation carriers = 10; non-carriers = 14) and fifteen patients with sporadic Alzheimer’s disease were included. The individuals underwent PET imaging with 11C-DED, 11C-PIB and 18F-FDG, as markers of reactive astrogliosis, amyloid-β deposition, and glucose metabolism, respectively, and plasma sampling for measuring GFAP concentrations. Twenty-one participants from the Autosomal Dominant Alzheimer’s Disease group underwent follow-up plasma sampling and ten of these participants underwent follow-up PET imaging. In mutation carriers, plasma GFAP levels and 11C-PIB binding increased, while 11C-DED binding and 18F-FDG uptake significantly decreased across the estimated years to symptom onset. Cross-sectionally, plasma GFAP demonstrated a negative correlation with 11C-DED binding in both mutation carriers and patients with sporadic disease. Plasma GFAP indicated cross-sectionally a significant positive correlation with 11C-PIB binding and a significant negative correlation with 18F-FDG in the whole sample. The longitudinal levels of 11C-DED binding showed a significant negative correlation with longitudinal plasma GFAP concentrations over the follow-up interval. Plasma GFAP concentration and astrocyte 11C-DED brain binding levels followed divergent trajectories and may reflect different underlying processes. The strong negative association between plasma GFAP and 11C-DED binding in Autosomal Dominant and sporadic Alzheimer’s disease brains may indicate that if both are markers of reactive astrogliosis, they may detect different states or subtypes of astrogliosis. Increased 11C-DED brain binding seems to be an earlier phenomenon in Alzheimer’s disease progression than increased plasma GFAP concentration.
      datePublished:2023-09-12T00:00:00Z
      dateModified:2023-09-12T00:00:00Z
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         Astrogliosis
         Deprenyl
         Plasma GFAP
         Alzheimer’s disease
         Astrocytes
         Autosomal Dominant Alzheimer’s disease
         Neurosciences
         Neurology
         Molecular Medicine
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         name:Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK
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         name:Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden
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      name:Karolinska University Hospital-Solna
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               name:Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden
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               name:Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden
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               type:PostalAddress
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            address:
               name:Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden
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            name:University College London
            address:
               name:Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK
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            address:
               name:UK Dementia Research Institute at UCL, London, UK
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            address:
               name:Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China
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            name:University of Wisconsin, University of Wisconsin-Madison
            address:
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      name:Caroline Graff
      affiliation:
            name:Karolinska Institutet
            address:
               name:Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden
               type:PostalAddress
            type:Organization
            name:Karolinska University Hospital-Solna
            address:
               name:Unit for Hereditary Dementia, Karolinska University Hospital-Solna, Solna, Sweden
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      name:Agneta Nordberg
      url:http://orcid.org/0000-0001-7345-5151
      affiliation:
            name:Karolinska Institutet
            address:
               name:Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden
               type:PostalAddress
            type:Organization
            name:Karolinska University Hospital
            address:
               name:Theme Inflammation and Aging, Karolinska University Hospital, Stockholm, Sweden
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden
      name:Department of Neurology, Karolinska University Hospital, Stockholm, Sweden
      name:Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden
      name:Theme Inflammation and Aging, Karolinska University Hospital, Stockholm, Sweden
      name:Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden
      name:Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden
      name:Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
      name:Centre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway
      name:Institute of Psychiatry, Psychology & Neuroscience, King’s College London, Maurice Wohl Clinical Neuroscience Institute, London, UK
      name:NIHR Biomedical Research Centre for Mental Health & Biomedical Research Unit for Dementia at South London & Maudsley NHS Foundation, London, UK
      name:Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
      name:Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden
      name:Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
      name:Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden
      name:Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK
      name:UK Dementia Research Institute at UCL, London, UK
      name:Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China
      name:Wisconsin Alzheimer’s Disease Research Center, School of Medicine and Public Health, University of Wisconsin, University of Wisconsin-Madison, Madison, USA
      name:Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden
      name:Unit for Hereditary Dementia, Karolinska University Hospital-Solna, Solna, Sweden
      name:Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden
      name:Theme Inflammation and Aging, Karolinska University Hospital, Stockholm, Sweden

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