Accelerated amyloid deposition in SARS-CoV-2 infected mouse models of Alzheimer’s disease DOI Creative Commons

Parag Parekh,

Andrew Badachhape, JeAnna R. Redd

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 10, 2024

Abstract Familial Alzheimer’s disease (AD) involving known AD causing genes accounts for a small fraction of cases, the vast majority are sporadic. Neuroinflammation, secondary to viral infection, has been suggested as an initiating or accelerating factor. In this work we tested hypothesis that SARS-CoV-2 (SCV2) infection accelerates development pathology in mouse models AD. We profiled transcriptomic changes using transgenic APP/PSEN1 and P301S develop k18hACE2 mice express humanized ACE2 receptor used by SCV2 enter cells. This study identified interferon chemokine responses constituting key shared pathways between pathology. Two AD: (develops amyloid pathology) 3xTg both tau were crossed with k18-hACE2 generate hybrid hACE2-3xTg hACE2-APP/PSEN1 mice. Neuroinflammation deposition brain infected imaged vivo molecular MRI (mMRI) probes confirmed postmortem histopathology. Results show 11-14-month-old exhibit neuroinflammation 10 days post 4–5-month-old hACE2-APP/PS1 deposits, while age-matched uninfected neither phenotype. suggests could induce accelerate when risk factors present.

Language: Английский

Exploring the Pathophysiology of Long COVID: The Central Role of Low-Grade Inflammation and Multisystem Involvement DOI Open Access
Evgeni Gusev, Alexey Sarapultsev

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(12), P. 6389 - 6389

Published: June 9, 2024

Long COVID (LC), also referred to as Post COVID-19 Condition, Post-Acute Sequelae of SARS-CoV-2 Infection (PASC), and other terms, represents a complex multisystem disease persisting after the acute phase COVID-19. Characterized by myriad symptoms across different organ systems, LC presents significant diagnostic management challenges. Central disorder is role low-grade inflammation, non-classical inflammatory response that contributes chronicity diversity observed. This review explores pathophysiological underpinnings LC, emphasizing importance inflammation core component. By delineating pathogenetic relationships clinical manifestations this article highlights necessity for an integrated approach employs both personalized medicine standardized protocols aimed at mitigating long-term consequences. The insights gained not only enhance our understanding but inform development therapeutic strategies could be applicable chronic conditions with similar features.

Language: Английский

Citations

8
Microfluidic Isolation of Neuronal-Enriched Extracellular Vesicles Shows Distinct and Common Neurological Proteins in Long COVID, HIV Infection and Alzheimer’s Disease DOI Open Access
Lynn Pulliam,

Bing Sun,

Erin McCafferty

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(7), P. 3830 - 3830

Published: March 29, 2024

Long COVID (LongC) is associated with a myriad of symptoms including cognitive impairment. We reported at the beginning COVID-19 pandemic that neuronal-enriched or L1CAM+ extracellular vesicles (nEVs) from people LongC contained proteins Alzheimer’s disease (AD). Since time, subset prior infection continue to report neurological problems more than three months after infection. Blood markers better characterize are elusive. To further identify neuronal LongC, we maximized number nEVs isolated plasma by developing hybrid EV Microfluidic Affinity Purification (EV-MAP) technique. and complaints, AD, HIV mild Using OLINK platform assesses 384 proteins, identified 11 significant increased in 2 decreased (BST1, GGT1). Fourteen were AD forty impairment elevated one (IVD). One common protein (BST1) was HIV. Six (MIF, ENO1, MESD, NUDT5, TNFSF14 FYB1) expressed both no AD. This study begins differences similarities response versus

Language: Английский

Citations

6
Role of toll-like receptors in post-COVID-19 associated neurodegenerative disorders? DOI Creative Commons
Senthil Kumaran Satyanarayanan, Tsz Fung Yip,

Zixu Han

et al.

Frontiers in Medicine, Journal Year: 2025, Volume and Issue: 12

Published: March 26, 2025

In the intricate realm of interactions between hosts and pathogens, Toll-like receptors (TLRs), which play a crucial role in innate immune response, possess ability to identify specific molecular signatures. This includes components originating from pathogens such as SARS-CoV-2, well resulting damage-associated patterns (DAMPs), endogenous molecules released after cellular damage. A developing perspective suggests that TLRs central neuroinflammation, fundamental factor neurodegenerative conditions like Alzheimer’s Parkinson’s disease (PD). comprehensive review consolidates current research investigating potential interplay TLRs, their signaling mechanisms, processes neurodegeneration following SARS-CoV-2 infection with an aim elucidate involvement long-term neurological complications COVID-19 explore targeting means implementing intervention strategies for prevention or treatment COVID-19-associated brain outcomes.

Language: Английский

Citations

0
Promising Strategies to Reduce the SARS-CoV-2 Amyloid Deposition in the Brain and Prevent COVID-19-Exacerbated Dementia and Alzheimer’s Disease DOI Creative Commons
Nikita Navolokin,

Viktoria Adushkina,

Daria Zlatogorskaya

et al.

Pharmaceuticals, Journal Year: 2024, Volume and Issue: 17(6), P. 788 - 788

Published: June 16, 2024

The COVID-19 pandemic, caused by infection with the SARS-CoV-2 virus, is associated cognitive impairment and Alzheimer’s disease (AD) progression. Once it enters brain, virus stimulates accumulation of amyloids in brain that are highly toxic to neural cells. These may trigger neurological symptoms COVID-19. meningeal lymphatic vessels (MLVs) play an important role removal toxins mediate viral drainage from brain. MLVs considered a promising target prevent COVID-19-exacerbated dementia. However, there limited methods for augmentation MLV function. This review highlights new discoveries field COVID-19-mediated amyloid development strategies stimulate clearance through other pathways. based on innovative treating dysfunction induced infection, including use photobiomodulation, plasmalogens, medicinal herbs, which offer hope addressing challenges posed virus.

Language: Английский

Citations

3
Non-canonical pathways associated to Amyloid beta and tau protein dyshomeostasis in Alzheimer’s disease: A narrative review DOI Creative Commons

Anna Maggiore,

Valentina Latina, Maria D’Erme

et al.

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 102, P. 102578 - 102578

Published: Nov. 13, 2024

Alzheimer's Disease (AD) is the most common form of dementia among elderly people. This disease imposes a significant burden on healthcare system, society, and economy due to increasing global aging population. Current trials with drugs or bioactive compounds aimed at reducing cerebral Amyloid beta (Aβ) plaques tau protein neurofibrillary tangles, which are two main hallmarks this devastating neurodegenerative disease, have not provided results in terms their neuropathological outcomes nor met expected clinical end-points. Ageing, genetic environmental risk factors, along different symptoms suggest that AD complex heterogeneous disorder multiple interconnected pathological pathways rather than single entity. In present review, we highlight discuss various non-canonical, Aβ-independent mechanisms, like gliosis, unhealthy dietary intake, lipid sugar signaling, cerebrovascular damage contribute onset development AD. We emphasize challenging traditional "amyloid cascade hypothesis" may improve our understanding age-related syndrome help fight progressive cognitive decline

Language: Английский

Citations

3
The Role of ACE2 in Neurological Disorders: From Underlying Mechanisms to the Neurological Impact of COVID-19 DOI Open Access
Jingwen Li, Xiangrui Kong, Tingting Liu

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(18), P. 9960 - 9960

Published: Sept. 15, 2024

Angiotensin-converting enzyme 2 (ACE2) has become a hot topic in neuroscience research recent years, especially the context of global COVID-19 pandemic, where its role neurological diseases received widespread attention. ACE2, as multifunctional metalloprotease, not only plays critical cardiovascular system but also an important protection, development, and inflammation regulation nervous system. The pandemic further highlights importance ACE2 SARS-CoV-2 enters host cells by binding to which may directly or indirectly affect system, leading range symptoms. This review aims explore function well potential impact therapeutic various diseases, providing new perspective for treatment disorders.

Language: Английский

Citations

2
Brain Mechanisms Involved in Post COVID Syndrome: A Narrative Review DOI Creative Commons

N. V. Gulyaeva

Neurochemical Journal, Journal Year: 2024, Volume and Issue: 18(3), P. 397 - 405

Published: Sept. 1, 2024

Language: Английский

Citations

1
Trends in Global Burden of Alzheimer’s Disease and Other Dementias Attributable to High Fasting Plasma Glucose, 1990–2021 DOI Creative Commons
Irena Ilić, Vladimir Jakovljević, Ivana Živanović-Mačužić

et al.

Medicina, Journal Year: 2024, Volume and Issue: 60(11), P. 1783 - 1783

Published: Oct. 31, 2024

: Alzheimer's disease and other dementias represent some of the leading public health concerns worldwide. This study aimed to assess global burden attributable high fasting plasma glucose in last decades.

Language: Английский

Citations

1
Changes in Private Psychiatric Outservice Related to SARS-CoV-2 Pandemic DOI Open Access
Marta Luigi,

Scognamiglio Rosamaria

Archives of Case Reports, Journal Year: 2024, Volume and Issue: 8(3), P. 121 - 125

Published: Nov. 8, 2024

The SARS-CoV-2 pandemic, which began in late 2019, initially manifested with acute respiratory symptoms, including bilateral pneumonia, and later emerged as a systemic disease. This brief report assesses changes the clinical profiles of psychiatric outpatients before, during, after pandemic’s most severe periods, focusing on mood, anxiety, cognitive symptoms. Data from private facility Rome reveal that both pandemic-related stressors infection itself may contribute to enduring affective symptoms older younger adult subgroups. Notably, during patients showed elevated psychopathology scores (BPRS-24) compared individuals. In post-pandemic period, adults exhibited increased positive PANSS Positive subscale, suggesting gradual worsening ( = 0.47). Cognitive assessments (MMSE PM38) further highlighted fluctuating performance over time, showing two distinct declines pandemic 2024. work underscores importance sustained mental health interventions address psychosocial neuroinflammatory legacy. perspective also considers new data CNS effects “toxin-like peptides” synthesized by microbiome bacteria.

Language: Английский

Citations

0
Accelerated amyloid deposition in SARS-CoV-2 infected mouse models of Alzheimer’s disease DOI Creative Commons

Parag Parekh,

Andrew Badachhape, JeAnna R. Redd

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 10, 2024

Abstract Familial Alzheimer’s disease (AD) involving known AD causing genes accounts for a small fraction of cases, the vast majority are sporadic. Neuroinflammation, secondary to viral infection, has been suggested as an initiating or accelerating factor. In this work we tested hypothesis that SARS-CoV-2 (SCV2) infection accelerates development pathology in mouse models AD. We profiled transcriptomic changes using transgenic APP/PSEN1 and P301S develop k18hACE2 mice express humanized ACE2 receptor used by SCV2 enter cells. This study identified interferon chemokine responses constituting key shared pathways between pathology. Two AD: (develops amyloid pathology) 3xTg both tau were crossed with k18-hACE2 generate hybrid hACE2-3xTg hACE2-APP/PSEN1 mice. Neuroinflammation deposition brain infected imaged vivo molecular MRI (mMRI) probes confirmed postmortem histopathology. Results show 11-14-month-old exhibit neuroinflammation 10 days post 4–5-month-old hACE2-APP/PS1 deposits, while age-matched uninfected neither phenotype. suggests could induce accelerate when risk factors present.

Language: Английский

Citations

0