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Updated: Jun 11, 2025

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
One immune cell to bind them all: platelet contribution to neurodegenerative disease
Gabriela Rodriguez Moore1, Isabel Melo-Escobar1,2, David Stegner3,4
1Department of Biology, University of Miami, Coral Gables, FL, 33146, USA.
Insights
Platelets, not just their count, are key in Alzheimer's disease (AD) and related dementias (ADRD). Altered platelet function and inflammation contribute to cognitive decline, offering new intervention targets.
Area of Science:
- Neuroscience
- Hematology
- Immunology
Background:
- Alzheimer's disease (AD) and related dementias (ADRD) significantly impact aging populations globally.
- AD pathology involves amyloid beta plaques, neurofibrillary tangles, vasculature issues, and chronic inflammation.
- Platelets are increasingly recognized for their roles in systemic and neuroinflammation.
Purpose of the Study:
- To review the critical roles of platelets in Alzheimer's disease (AD) and related dementias (ADRD).
- To explore how platelet receptors, secreted molecules, and inflammatory interactions contribute to ADRD pathogenesis.
- To highlight the potential of targeting platelet function for ADRD management and intervention.
Main Methods:
- Review of recent scientific literature on platelets in AD and ADRD.
- Analysis of studies investigating platelet receptor expression and activation in AD patients.
- Examination of platelet granule contents and their relation to AD pathology.
Main Results:
- Altered platelet receptor expression correlates with accelerated cognitive decline in AD patients.
- Platelets from AD patients show heightened unstimulated activation.
- Platelet dysregulation, not quantity, is linked to increased risk of bleeding, stroke, and cognitive decline.
Conclusions:
- Platelet-mediated inflammation and healing disruptions are hypothesized to be crucial in ADRD development.
- Platelets' receptors, secreted molecules, and inflammatory interactions offer promising avenues for ADRD management.
- Understanding platelet roles provides new perspectives for therapeutic interventions in ADRD.
Abstract:
Alzheimer's disease (AD) and related dementias (ADRD) collectively affect a significant portion of the aging population worldwide. The pathological progression of AD involves not only the classical hallmarks of amyloid beta (Aβ) plaque buildup and neurofibrillary tangle development but also the effects of vasculature and chronic inflammatory processes. Recently, platelets have emerged as central players in systemic and neuroinflammation. Studies have shown that patients with altered platelet receptor expression exhibit accelerated cognitive decline independent of traditional risk factors. Additionally, platelets from AD patients exhibit heightened unstimulated activation compared to control groups. Platelet granules contain crucial AD-related proteins like tau and amyloid precursor protein (APP). Dysregulation of platelet exocytosis contributes to disease phenotypes characterized by increased bleeding, stroke, and cognitive decline risk. Recent studies have indicated that these effects are not associated with the quantity of platelets present in circulation. This underscores the hypothesis that disruptions in platelet-mediated inflammation and healing processes may play a crucial role in the development of ADRD. A thorough look at platelets, encompassing their receptors, secreted molecules, and diverse roles in inflammatory interactions with other cells in the circulatory system in AD and ADRD, holds promising prospects for disease management and intervention. This review discusses the pivotal roles of platelets in ADRD.
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