Biomarkers.

Background: The heterogeneous etiology of "sporadic" Alzheimer's disease (sAD) includes genetic influences. To better understand synaptic dysfunction in AD pathogenesis, we used protein quantitative train loci (pQTL) assessments and a polygenic risk score (PRS) to examine the relationship between synaptic integrity and longitudinal cognitive performance in the presymptomatic phase of the disease.

Method: The PREVENT-AD cohort includes symptom-free elderly participants at risk of AD because of their family history.

Biomarkers.

Background: Synaptic dysfunction plays an important role in Alzheimer's disease (AD) and cognitive decline. We investigated the association between cerebrospinal fluid (CSF) synaptic protein levels and quantitative EEG (qEEG) measures, two modalities to measure synaptic dysfunction in AD pathology. We assessed combined and independent prognostic value of both modalities for cognitive decline along the AD continuum.

Biomarkers.

Background: The immune complement system is key to the elimination of redundant neural connections in the brain through a process called synaptic pruning. In neurodegenerative diseases such as Alzheimer's disease (AD), this system may result in excessive synapse loss, leading to brain atrophy and cognitive impairment. While increased cerebrospinal fluid (CSF) levels of complement proteins have been observed in patients with AD dementia, no studies have yet investigated the role of complement in the pre-symptomatic phase of AD, nor throughout its progression.

Biomarkers.

Background: Synapse loss in Alzheimer's disease (AD) is correlates closely with cognitive impairment. Recent evidence suggests that synapse loss is promoted by amyloid-beta, leading in turn to the spread of tau pathology. We sought to assess: 1) the association in positron emission tomography (PET) between several cerebrospinal fluid (CSF) synaptic biomarkers and amyloid and tau burden, as well as their annual change; and 2) the potential clinical utility of these synaptic biomarkers in preclinical AD.

Biomarkers.

Background: Leukocyte telomere length (LTL) serves as a proxy for tissue-specific TL and peripheral immune aging. Its association with aging-related brain endophenotypes, cognitive functioning, and Alzheimer's disease (AD) risk is established, but the underlying molecular mechanisms remain elusive. Investigating LTL's association with AD biomarkers is crucial for identifying its role in brain resilience and disease progression.