Is amyloid involved in acute neuroinflammation? A CSF analysis in encephalitis

Padovani, Alessandro; Canale, Antonio; Schiavon, Lorenzo; Masciocchi, Stefano; Imarisio, Alberto; Risi, Barbara; Bonzi, Giulio; Giuli, Valeria De; Luca, Mónica Di; Ashton, Nicholas J.; Blennow, Kaj; Zetterberg, Henrik; Pilotto, Andrea

doi:10.1002/alz.12554

Cited by 4 publications

(1 citation statement)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In studies in transgenic mouse models of AD, the release of TNF from microglia in response to Ab is triggered by the interaction of CD40 with CD40L or by the involvement of TLR4 (75). Recent studies have found higher levels of inflammatory cytokines and neuronal/glial markers in the cerebrospinal fluid of patients with acute neuritis compared to controls, with no differences in amyloid-related markers (76). Together, the above studies suggest an association between neuroinflammation and AD.…”

Section: Neuroinflammation In Diseases Of the Central Nervous Systemmentioning

confidence: 90%

Platelets, Thromboinflammation and Neurovascular Disease

Sun

Langer

2022

Front. Immunol.

View full text Add to dashboard Cite

The brain and spinal cord are immune-privileged organs, but in the disease state protection mechanisms such as the blood brain barrier (BBB) are ineffective or overcome by pathological processes. In neuroinflammatory diseases, microglia cells and other resident immune cells contribute to local vascular inflammation and potentially a systemic inflammatory response taking place in parallel. Microglia cells interact with other cells impacting on the integrity of the BBB and propagate the inflammatory response through the release of inflammatory signals. Here, we discuss the activation and response mechanisms of innate and adaptive immune processes in response to neuroinflammation. Furthermore, the clinical importance of neuroinflammatory mediators and a potential translational relevance of involved mechanisms are addressed also with focus on non-classical immune cells including microglia cells or platelets. As illustrative examples, novel agents such as Anfibatide or Revacept, which result in reduced recruitment and activation of platelets, a subsequently blunted activation of the coagulation cascade and further inflammatory process, demonstrating that mechanisms of neuroinflammation and thrombosis are interconnected and should be further subject to in depth clinical and basic research.

show abstract

Section: Neuroinflammation In Diseases Of the Central Nervous Systemmentioning

confidence: 90%

Platelets, Thromboinflammation and Neurovascular Disease

Sun

Langer

2022

Front. Immunol.

View full text Add to dashboard Cite

show abstract

Is amyloid involved in acute neuroinflammation? A CSF analysis in encephalitis

Padovani

Canale

Schiavon

et al. 2022

Alzheimer's & Dementia

View full text Add to dashboard Cite

Introduction: Several investigations have argued for a strong relationship between neuroinflammation and amyloid metabolism but it is still unclear whether inflammation exerts a pro-amyloidogenic effect, amplifies the neurotoxic effect of amyloid, or is protective.Methods: Forty-two patients with acute encephalitis (ENC) and 18 controls underwent an extended cerebrospinal fluid (CSF) panel of inflammatory, amyloid (Aβ40, 42, and 38, sAPP-α, sAPP-β), glial, and neuronal biomarkers. Linear and non-linear correlations between CSF biomarkers were evaluated studying conditional independence relationships.Results: CSF levels of inflammatory cytokines and neuronal/glial markers were higher in ENC compared to controls, whereas the levels of amyloid-related markers did not differ. Inflammatory markers were not associated with amyloid markers but exhibited a correlation with glial and neuronal markers in conditional independence analysis.Discussion: By an extensive CSF biomarkers analysis, this study showed that an acute neuroinflammation state, which is associated with glial activation and neuronal damage, does not influence amyloid homeostasis.

show abstract