The number of patients with Alzheimer’s disease(AD)is increasing worldwide due to extended life expectancy,with AD being the most common cause of dementia.AD pathological hallmarks consist of brain depositions of agg...The number of patients with Alzheimer’s disease(AD)is increasing worldwide due to extended life expectancy,with AD being the most common cause of dementia.AD pathological hallmarks consist of brain depositions of aggregated amyloid beta(Aβ)into neuritic plaques and neurofibrillary tangles of hyperphosphorylated tau,lead-ing to synaptic dysfunction and neuronal loss[1].Prot-eomic studies of cerebrospinal fluid(CSF)have shown that several biological processes are dysregulated in AD,such as the innate immune system,inflammatory response,hemostasis,lipid processing,oxidative stress response and synaptic functioning[2].展开更多
基金funded by the Portuguese Science and Technology Foundation(FCT)Beyond Beta Amyloid:Deciphering Early Pathogenic Changes in Alzheimer’s disease project PTDC/MED-NEU/27946/2017,by The National Mass Spectrometry Network(POCI-01–0145-FEDER-402–022125 Ref.ROTEIRO/0028/2013),UIDB/04539/2020,UIDP/04539/2020,through funding of LASIGE Research Unit(UIDB/00408/2020 and UIDP/00408/2020).
文摘The number of patients with Alzheimer’s disease(AD)is increasing worldwide due to extended life expectancy,with AD being the most common cause of dementia.AD pathological hallmarks consist of brain depositions of aggregated amyloid beta(Aβ)into neuritic plaques and neurofibrillary tangles of hyperphosphorylated tau,lead-ing to synaptic dysfunction and neuronal loss[1].Prot-eomic studies of cerebrospinal fluid(CSF)have shown that several biological processes are dysregulated in AD,such as the innate immune system,inflammatory response,hemostasis,lipid processing,oxidative stress response and synaptic functioning[2].
