Publications by authors named "E Kontsekova"

Article Synopsis
  • Tau pathology is closely linked to cognitive decline in Alzheimer's disease (AD), prompting the development of tau-targeting immunotherapies like AADvac1, aimed at halting disease progression.
  • The ADAMANT clinical trial evaluated AADvac1 in a subgroup of mild AD participants with elevated plasma p-tau217 levels over 24 months, focusing on safety and several cognitive and biological outcome measures.
  • Results showed AADvac1 was safe and well-tolerated, significantly reduced levels of plasma neurofilament light and glial fibrillary acidic protein, and had a favorable—though not statistically significant—impact on cognitive scores and brain tissue preservation in certain regions, particularly in older participants.
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Background: Tau pathology correlates with and predicts clinical decline in Alzheimer's disease. Approved tau-targeted therapies are not available.

Methods: ADAMANT, a 24-month randomised, placebo-controlled, parallel-group, double-blinded, multicenter, Phase 2 clinical trial (EudraCT2015-000630-30, NCT02579252) enrolled 196 participants with Alzheimer's disease; 119 are included in this post-hoc subgroup analysis.

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COVID-19 and especially Long COVID are associated with severe CNS symptoms and may place persons at risk to develop long-term cognitive impairments. Here, we show that two non-infective models of SARS-CoV-2 can cross the blood-brain barrier (BBB) and induce neuroinflammation, a major mechanism underpinning CNS and cognitive impairments, even in the absence of productive infection. The viral models cross the BBB by the mechanism of adsorptive transcytosis with the sugar N-acetylglucosamine being key.

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Alzheimer's disease (AD) is an age-related neurodegenerative disease characterized by progressive memory decline, histopathological lesions such as amyloid β plaques and neurofibrillary tangles, and neuroinflammation driven by glial cells. Microglia, the innate immune cells of the brain, dynamically survey their environment for signs of infection and cell damage. Although our understanding of microglia and their modes of activation has expanded in recent years, their role in AD is still not completely understood.

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