Synaptic dysfunction represents an early pathological event that precedes neurodegeneration in Alzheimer’s disease(AD),even though the molecular mechanisms that underlie synaptic dysfunction remain to be completely u...Synaptic dysfunction represents an early pathological event that precedes neurodegeneration in Alzheimer’s disease(AD),even though the molecular mechanisms that underlie synaptic dysfunction remain to be completely understood[1,2].Nonetheless,in vivo synaptic biomarkers are highly relevant as they have the potential to reveal early-stage changes and to track target engagement of specific disease-modifying strategies.A range of cerebrospinal fluid(CSF)synapse-related biomarkers including neurogranin,GAP43,SNAP25,neuregulin-1,PSD-95 and neuronal pentraxin have indeed been reported in AD at variance with other dementing illnesses[1–3].展开更多
基金Alessandro Padovani received grant from the the Italian Ministry of University and Research PRIN COCOON(2017MYJ5TH)and PRIN 2021 RePlast(PRIN202039WMFP)the H2020 IMI IDEA-FAST(ID853981)+12 种基金Italian Ministry of Health Grant/Award Number:RF-2018-12366209PNRR-Health PNRRMAD-2022-12376110from CARIPLO Foundation.APi has been supported by grants from Airalzh Foundation AGYR2021 Life-Bio Grant,The LIMPEDISMOV Foundation Segala Grant 2021,the Italian Ministry of University and Research PRIN COCOON(2017MYJ5TH),PRIN 2021 RePlast(PRIN202039WMFP)from Italian Ministry of Enterprises and Made in Italy(PNRR-Next generation EU funding,PRIN)the H2020 IMI IDEA-FAST(ID853981)Italian Ministry of Health,Grant/PRIN2022 PNRR P2022TKN8C.Silvia Pelucchi is supported by Piano di sostegno alla ricerca(PSR)PSR2022_DIP_022_AZIONE_A_SPELU.Laura D’Andrea reports no competing interest.Ramona Stringhi reports no competing interest.Federica Gorla reports no competing interest.Bahar Aksan reports no competing interest.Salvatore Caratozzolo reports no competing interest.Alberto Benussi was partially supported by Fondazione Cariplo(grant no 2021-1516)by the Fondation pour la Recherche sur Alzheimer.Alice Galli reports no conflict of interest.Clara Tirloni reports no conclict of interest.Daniela Mauceri received grant support from the Alzheimer Forschung Initiative(Grant no.21019)the Chica and Heinz Schaller Foundation,German Research Foundation(Deutsche ForschungsgemeinschaftSFB1158 project A08)Antonio Canale reports no competing interest.Silvana Archetti reports no competing interest.Barbara Borroni reports grant support from Ministry of Health(MINSAL)and Ministry of Education,Research and University(MIUR),and from CARIPLO Foundation.Monica Di Luca received grant support from Italian Ministry of Health(MINSAL)and Italian Ministry of Research and University(MUR)(grant numbers PRIN 20202THZAW and PRIN2022 PNRR P2022TKN8C,FIS00000560-Stone,PNRR,Missione 4-Componente 2-Investimento 1.3,finanziato dall’Unione europea-NextGenerationEU“Fascination”)Elena Marcello received grant support from Italian Ministry of Research and University(MUR)(PRIN202039WMFP and PRIN2022 PNRR P2022R2E8N)from the Giovanni Armenise Harvard Foundation and AIRALZH ONLUS(2023 Armenise Harvard-AIRALZH Mid-Career Award in Neurodegenerative Diseases-AHA MCA)from Italian Ministry of Enterprises and Made in Italy(PNRR-Next generation EU funding,“SEED for Innovation Patent 2.0”program,project TT_MIN23_SEED4IP2.0_07 to EM).
文摘Synaptic dysfunction represents an early pathological event that precedes neurodegeneration in Alzheimer’s disease(AD),even though the molecular mechanisms that underlie synaptic dysfunction remain to be completely understood[1,2].Nonetheless,in vivo synaptic biomarkers are highly relevant as they have the potential to reveal early-stage changes and to track target engagement of specific disease-modifying strategies.A range of cerebrospinal fluid(CSF)synapse-related biomarkers including neurogranin,GAP43,SNAP25,neuregulin-1,PSD-95 and neuronal pentraxin have indeed been reported in AD at variance with other dementing illnesses[1–3].
