Cyclosporine A (CsA) prevents synaptic impairment caused by truncated tau by caspase-3

Tapia-Monsalves, Carola; Olesen, Margrethe A.; Villavicencio-Tejo, Francisca; Quintanilla, Rodrigo A.

doi:10.1016/j.mcn.2023.103861

Cited by 5 publications

(3 citation statements)

References 98 publications

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“…7a ). Interestingly, they included genes, such as Lcn2 and Casp3 , that are linked to neurotoxicity 67 , 68 as well as others, such as Ralbp1 and Apoe , that are involved in dampening Alzheimer’s disease (AD)-related mitochondrial dysfunction or degradation of amyloid-beta 69 , 70 . In Tph cells, 19 such common genes were identified (Supplementary Fig.…”

Section: Resultsmentioning

confidence: 99%

Myelin-reactive B cells exacerbate CD4+ T cell-driven CNS autoimmunity in an IL-23-dependent manner

Fazazi,

Doss,

Pereira

et al. 2024

Nat Commun

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B cells and T cells collaborate in multiple sclerosis (MS) pathogenesis. IgH[MOG] mice possess a B cell repertoire skewed to recognize myelin oligodendrocyte glycoprotein (MOG). Here, we show that upon immunization with the T cell-obligate autoantigen, MOG[35-55], IgH[MOG] mice develop rapid and exacerbated experimental autoimmune encephalomyelitis (EAE) relative to wildtype (WT) counterparts, characterized by aggregation of T and B cells in the IgH[MOG] meninges and by CD4+ T helper 17 (Th17) cells in the CNS. Production of the Th17 maintenance factor IL-23 is observed from IgH[MOG] CNS-infiltrating and meningeal B cells, and in vivo blockade of IL-23p19 attenuates disease severity in IgH[MOG] mice. In the CNS parenchyma and dura mater of IgH[MOG] mice, we observe an increased frequency of CD4+PD-1+CXCR5- T cells that share numerous characteristics with the recently described T peripheral helper (Tph) cell subset. Further, CNS-infiltrating B and Tph cells from IgH[MOG] mice show increased reactive oxygen species (ROS) production. Meningeal inflammation, Tph-like cell accumulation in the CNS and B/Tph cell production of ROS were all reduced upon p19 blockade. Altogether, MOG-specific B cells promote autoimmune inflammation of the CNS parenchyma and meninges in an IL-23-dependent manner.

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Section: Resultsmentioning

confidence: 99%

Myelin-reactive B cells exacerbate CD4+ T cell-driven CNS autoimmunity in an IL-23-dependent manner

Fazazi,

Doss,

Pereira

et al. 2024

Nat Commun

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“…Therefore, immunomodulators are also receiving attention for their potential in the prevention and treatment of cognitive dysfunction. For example, some studies have found that the use of immunosuppressants like cyclosporine A and azathioprine can alleviate cognitive dysfunction ( Dobrowolski et al, 2023 ; Tapia-Monsalves et al, 2023 ).…”

Section: Some Preventive Strategies For the Peripheral Inflammation P...mentioning

confidence: 99%

Peripheral inflammation as a potential mechanism and preventive strategy for perioperative neurocognitive disorder under general anesthesia and surgery

Li,

Fang

et al. 2024

Front. Cell. Neurosci.

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General anesthesia, as a commonly used medical intervention, has been widely applied during surgical procedures to ensure rapid loss of consciousness and pain relief for patients. However, recent research suggests that general anesthesia may be associated with the occurrence of perioperative neurocognitive disorder (PND). PND is characterized by a decline in cognitive function after surgery, including impairments in attention, memory, learning, and executive functions. With the increasing trend of population aging, the burden of PND on patients and society’s health and economy is becoming more evident. Currently, the clinical consensus tends to believe that peripheral inflammation is involved in the pathogenesis of PND, providing strong support for further investigating the mechanisms and prevention of PND.

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“…All these synaptic changes could be prevented by cyclosporine A, a drug which could inhibit the function of mitochondrial permeability transition pore (mPTP). It means that mPTP may play a role in synaptic dysfunction derived from caspase-3-cleaved tauΔD421, and cyclosporine A may have a cure for AD and other neural dysfunctional diseases [ 163 ].…”

Section: Role Of Tau Fragments In Neurodegenerationmentioning

confidence: 99%

Complicated Role of Post-translational Modification and Protease-Cleaved Fragments of Tau in Alzheimer’s Disease and Other Tauopathies

Yang,

Shen,

Shen

et al. 2023

Mol Neurobiol

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Tau, a microtubule-associated protein predominantly localized in neuronal axons, plays a crucial role in promoting microtubule assembly, stabilizing their structure, and participating in axonal transport. Perturbations in tau’s structure and function are implicated in the pathogenesis of neurodegenerative diseases collectively known as tauopathies, the most common disorder of which is Alzheimer’s disease (AD). In tauopathies, it has been found that tau has a variety of post-translational modification (PTM) abnormalities and/or tau is cleaved into a variety of fragments by some specific proteolytic enzymes; however, the precise contributions of these abnormal modifications and fragments to disease onset and progression remain incompletely understood. Herein, we provide an overview about the involvement of distinctive abnormal tau PTMs and different tau fragments in the pathogenesis of AD and other tauopathies and discuss the involvement of proteolytic enzymes such as caspases, calpains, and asparagine endopeptidase in mediating tau cleavage while also addressing the intercellular transmission role played by tau. We anticipate that further exploration into PTMs and fragmented forms of tau will yield valuable insights for diagnostic approaches and therapeutic interventions targeting AD and other related disorders.

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Cyclosporine A (CsA) prevents synaptic impairment caused by truncated tau by caspase-3

Cited by 5 publications

References 98 publications

Myelin-reactive B cells exacerbate CD4+ T cell-driven CNS autoimmunity in an IL-23-dependent manner

Myelin-reactive B cells exacerbate CD4+ T cell-driven CNS autoimmunity in an IL-23-dependent manner

Peripheral inflammation as a potential mechanism and preventive strategy for perioperative neurocognitive disorder under general anesthesia and surgery

Complicated Role of Post-translational Modification and Protease-Cleaved Fragments of Tau in Alzheimer’s Disease and Other Tauopathies

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