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O1‐11‐02: Combination of Cerebrospinal Fluid H‐FABP and Core Alzheimer's Disease Biomarkers Improves the Differential Diagnosis of Neurodegenerative Disorders
Author(s) -
Biscetti Leonardo,
Eusebi Paolo,
Salvadori Nicola,
Frattini Giulia,
Simoni Simone,
Mollenhauer Brit,
Engelborghs Sebastiaan,
Tambasco Nicola,
Calabresi Paolo,
Parnetti Lucilla,
Chiasserini Davide
Publication year - 2016
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2016.06.353
Subject(s) - dementia with lewy bodies , cerebrospinal fluid , biomarker , dementia , neurodegeneration , medicine , parkinson's disease , cognitive decline , gastroenterology , tau protein , pathology , disease , alzheimer's disease , biology , biochemistry
Background:Cognitive deficits are common clinical signs of depression and AD. Biomarkers may help to distinguish between early stages of AD and depression not associated with AD. Recently, cerebrospinal (CSF) levels of the synaptic proteins neurogranin and BACE1 have shown potential as progression markers for AD. Here, we analyzed CSF neurogranin, as well as CSF levels of the protein BACE1, in AD and depressed patients with and without cognitive deficits. Methods: We used research prototype ELISAs for measuring neurogranin and BACE1 in CSF of mild (n1⁄421) and moderate (n1⁄419) AD patients and depressed patients with (n1⁄420) or without (n1⁄420) cognitive malfunction. We also quantified CSF levels of Ab(1-38), Ab(1-40), Ab(1-42) and total-tau. Cognitive performance was tested by the CERAD test battery. Results:As expected, we found significantly increased CSF levels of neurogranin and BACE1 in moderate AD patients compared to depressed patients without cognitive deficits. Neurogranin CSF levels were already significantly increased in mild AD. Interestingly, the ratio of neurogranin/BACE1 enhanced the discrimination between mild AD and depression. Moreover, the ratio also significantly distinguished between mild AD and depression with cognitive deficits. For none of the analytes, significant differences were noted between both groups of depressed patients, although we saw a trend of increased CSF levels of neurogranin, BACE1 and tau. Finally, BACE1 and neurogranin were highly correlated in all groups.Conclusions:Neurogranin and BACE1 can be reliably detected in CSF of depressed and AD patients and might serve as biomarkers to facilitate clinical assignment of cognitive dysfunction. It would be valuable to assess the CSF neurogranin/BACE1 ratio in remitted formerly depressed patients via longitudinally sampling, to determine whether this ratio changes over time and correlates with clinical deterioration of cognition.