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Objective  Frontotemporal lobar degeneration ( FTLD ) is the second most prevalent dementia in young patients and is characterized by the presence of two main protein aggregates in the brain, tau ( FTLD ‐Tau) or  TDP 43 ( FTLD ‐ TDP ), which likely require distinct pharmacological therapy. However, specific diagnosis of  FTLD  and its subtypes remains challenging due to largely overlapping clinical phenotypes. Here, we aimed to assess the clinical performance of novel cerebrospinal fluid ( CSF ) biomarkers for discrimination of  FTLD  and its pathological subtypes.    Methods   YKL 40,  FABP 4,  MFG ‐E8, and the activities of catalase and specific lysosomal enzymes were analyzed in patients with  FTLD ‐ TDP  ( n  = 30),  FTLD ‐Tau ( n  = 20),  AD  ( n  = 30),  DLB  ( n  = 29), and nondemented controls ( n  = 29) obtained from two different centers. Models were validated in an independent  CSF  cohort ( n  = 188).    Results   YKL 40 and catalase activity were increased in  FTLD ‐ TDP  cases compared to controls.  YKL 40 levels were also higher in  FTLD ‐ TDP  compared to  FTLD ‐Tau. We identified biomarker models able to discriminate  FTLD  from nondemented controls ( MFG ‐E8,  tT au, and A β  42 ; 78% sensitivity and 83% specificity) and non‐ FTLD  dementia ( YKL 40,  pT au, p/ tT au ratio, and age; 90% sensitivity, 78% specificity), which were validated in an independent cohort. In addition, we identified a biomarker model differentiating  FTLD ‐ TDP  from  FTLD ‐Tau ( YKL 40,  MFGE ‐8,  β HexA together with  β HexA/ tH ex and p/ tT au ratios and age) with 80% sensitivity and 82% specificity.    Interpretation  This study identifies  CSF  protein signatures distinguishing  FTLD  and the two main pathological subtypes with optimal accuracy (specificity/sensitivity > 80%). Validation of these models may allow appropriate selection of cases for clinical trials targeting the accumulation of Tau or  TDP 43, thereby increasing their efficiency and facilitating the development of successful therapies.

Novel CSF biomarkers to discriminate FTLD and its pathological subtypes