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Biomarkers.
Alzheimers Dement
December 2024
Florey Institute of Neuroscience and Mental Health, Parkville, VIC, Australia.
Background: In Alzheimer's disease (AD), a major gap remains in the understanding of how the interplay between peripheral and central immune systems drives neuroinflammation and disease progression. More recently, the concept of brain lymph drainage has sparked interest as it may shed light on how the dynamics of T cell interactions contribute to AD. Our preliminary study aims to characterize alterations in the peripheral blood lymphocyte population among individuals with AD-dementia and mild cognitive impairment (MCI), as compared with cognitively unimpaired (CU) individuals.
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Alzheimers Dement
December 2024
Centro de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable (CIBERFES), Madrid, Spain.
Background: Detecting Alzheimer's disease (AD) biological hallmarks before clinical symptoms emerge is now possible with available blood-based biomarkers. However, the rate of cognitive decline varies among individuals at risk of AD, and accurate prognostic blood-based biomarkers are lacking. Our goal is to identify plasma proteins predictive of fast cognitive decline in asymptomatic individuals at risk of AD.
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Alzheimers Dement
December 2024
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Gothenburg, Sweden.
Background: Emerging evidence underscores the importance of neuroinflammation in the progression of Alzheimer's disease (AD) pathophysiology. Recent studies indicate the involvement of the inflammatory mechanisms both in amyloid- β (Aβ) and tau deposition in the brain. Nevertheless, due to the complexity of the immune responses and the intricate interplay between the peripheral and the central nervous systems, identifying biomarkers that reflect the brain´s inflammatory state in AD has been a challenge.
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Alzheimers Dement
December 2024
Department of Psychiatry, McGill University, Montréal, QC, Canada.
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.
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Alzheimers Dement
December 2024
Alzheimer's disease and other cognitive disorders unit, Hospital Clínic, IDIBAPS, Barcelona, Spain.
Background: Sleep-wake alterations are common symptoms in Alzheimer's Disease (AD) associated with faster cognitive decline. Noradrenaline dysfunction and neuroinflammation have been proposed as potential driving mechanisms. The ADIS project aims to study the relationship between sleep-wake patterns, immune signatures (peripheral blood cytotoxic lymphocytes), and noradrenergic markers across the AD spectrum.
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