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Are neuropsychiatric symptoms in dementia linked to CSF biomarkers of synaptic and axonal degeneration?
Department of Neurobiology, Caring Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden; Department of Dermatology, Karolinska University Hospital, Solna, Sweden.
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; UK Dementia Research Institute at UCL, London, UK; Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK.
Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; Center for Age-Related Diseases, Stavanger University Hospital, Stavanger, Norway.
Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
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2020 (English)In: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Vol. 12, no 1, article id 153Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: The underlying disease mechanism of neuropsychiatric symptoms (NPS) in dementia remains unclear. Cerebrospinal fluid (CSF) biomarkers for synaptic and axonal degeneration may provide novel neuropathological information for their occurrence. The aim was to investigate the relationship between NPS and CSF biomarkers for synaptic (neurogranin [Ng], growth-associated protein 43 [GAP-43]) and axonal (neurofilament light [NFL]) injury in patients with dementia.

METHODS: A total of 151 patients (mean age ± SD, 73.5 ± 11.0, females n = 92 [61%]) were included, of which 64 had Alzheimer's disease (AD) (34 with high NPS, i.e., Neuropsychiatric Inventory (NPI) score > 10 and 30 with low levels of NPS) and 18 were diagnosed with vascular dementia (VaD), 27 with mixed dementia (MIX), 12 with mild cognitive impairment (MCI), and 30 with subjective cognitive impairment (SCI). NPS were primarily assessed using the NPI. CSF samples were analyzed using enzyme-linked immunosorbent assays (ELISAs) for T-tau, P-tau, Aβ1-42, Ng, NFL, and GAP-43.

RESULTS: No significant differences were seen in the CSF levels of Ng, GAP-43, and NFL between AD patients with high vs low levels of NPS (but almost significantly decreased for Ng in AD patients < 70 years with high NPS, p = 0.06). No significant associations between NPS and CSF biomarkers were seen in AD patients. In VaD (n = 17), negative correlations were found between GAP-43, Ng, NFL, and NPS.

CONCLUSION: Our results could suggest that low levels of Ng may be associated with higher severity of NPS early in the AD continuum (age < 70). Furthermore, our data may indicate a potential relationship between the presence of NPS and synaptic as well as axonal degeneration in the setting of VaD pathology.

Place, publisher, year, edition, pages
BioMed Central, 2020. Vol. 12, no 1, article id 153
Keywords [en]
Alzheimer’s disease, CSF biomarkers, GAP-43, NPS, Neurofilament, Neurogranin, Synaptic and axonal dysfunction
National Category
Neurology
Identifiers
URN: urn:nbn:se:oru:diva-87481DOI: 10.1186/s13195-020-00718-yISI: 000594633600002PubMedID: 33203439Scopus ID: 2-s2.0-85096132731OAI: oai:DiVA.org:oru-87481DiVA, id: diva2:1502627
Funder
Swedish Research Council, 2018-02532 2018-02843The Swedish Brain Foundation, FO2019-0140 FO2018-0315Stiftelsen Gamla TjänarinnorThe Karolinska Institutet's Research Foundation
Note

Funding Agencies:

National Institute for Health Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London 

European Research Council (ERC)681712

Swedish State Support for Clinical Research ALFGBG-720931

UK Dementia Research Institute at UCL  

Stohnes Stiftelse  

Sarfond 31 Forskning Senil demens 

Demensfonden 

Available from: 2020-11-20 Created: 2020-11-20 Last updated: 2021-01-14Bibliographically approved

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