Dataset Information

The Neuroinflammasome in Alzheimer's Disease and Cerebral Stroke.

ABSTRACT:

Aim/background

This review investigated a patient with Alzheimer's disease (AD) treated with 4,4'-diaminodiphenyl sulfone (DDS) as a neuroinflammasome competitor.

Methods

We monitored AD's progression through numeric clinical staging (NCS) with a new biomarker. NCS was determined by the presence of AD symptoms and neuropsychiatric (NP) symptoms caused by anti-AD (AAD) drugs (D) as a biomarker. We also monitored the function of DDS for stroke in a no-intake emergency state.

Results

By introducing (D), AD's progression was monitored through NCS staging. AAD side effects and neuropsychiatric symptoms were identified. DDS was stopped in patients with stroke with NCS 6 caused by AAD, and it rapidly proceeded to cerebral infarct.

Conclusions

AAD can occasionally exacerbate AD and stroke. DDS can alleviate mild cognitive impairment (MCI), early AD and stroke. We clinically confirmed the role of DDS as a neuroinflammasome competitor after stroke. DDS preserved neuronal survival within 24-55 h in the Seoul Study cohort.

SUBMITTER: Lee JH

PROVIDER: S-EPMC8255751 | biostudies-literature | 2021 May-Aug

REPOSITORIES: biostudies-literature

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Publications

The Neuroinflammasome in Alzheimer's Disease and Cerebral Stroke.

Lee Jong-Hoon JH Lee Chul Joong CJ Park Jungwuk J Lee So Jeong SJ Choi Su-Hee SH

Dementia and geriatric cognitive disorders extra 20210501 2

<h4>Aim/background</h4>This review investigated a patient with Alzheimer's disease (AD) treated with 4,4'-diaminodiphenyl sulfone (DDS) as a neuroinflammasome competitor.<h4>Methods</h4>We monitored AD's progression through numeric clinical staging (NCS) with a new biomarker. NCS was determined by the presence of AD symptoms and neuropsychiatric (NP) symptoms caused by anti-AD (AAD) drugs (D) as a biomarker. We also monitored the function of DDS for stroke in a no-intake emergency state.<h4>Resu ...[more]

PMID: 34249072

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Project description:Neuronal dysfunction in specific brain regions or across distributed brain networks is a known feature of Alzheimer's disease. An often reported finding in the early stage of the disease is the presence of increased functional MRI (fMRI) blood oxygenation level-dependent signal under task conditions relative to cognitively normal controls, a phenomenon known as 'hyperactivation'. However, research in the past decades yielded complex, sometimes conflicting results. The magnitude and topology of fMRI hyperactivation patterns have been found to vary across the preclinical and clinical spectrum of Alzheimer's disease, including concomitant 'hypoactivation' in some cases. These incongruences are likely due to a range of factors, including the disease stage at which the cohort is examined, the brain areas or networks studied and the fMRI paradigm utilized to evoke these functional abnormalities. Additionally, a perennial question pertains to the nature of hyperactivation in the context of Alzheimer's disease. Some propose it reflects compensatory mechanisms to sustain cognitive performance, while others suggest it is linked to the pathological disruption of a highly regulated homeostatic cycle that contributes to, or even drives, disease progression. Providing a coherent narrative for these empirical and conceptual discrepancies is paramount to develop disease models, understand the synergy between hyperactivation and the Alzheimer's disease pathological cascade and tailor effective interventions. We first provide a comprehensive overview of functional brain changes spanning the course from normal ageing to the clinical spectrum of Alzheimer's disease. We then highlight evidence supporting a close relationship between fMRI hyperactivation and in vivo markers of Alzheimer's pathology. We primarily focus on task-based fMRI studies in humans, but also consider studies using different functional imaging techniques and animal models. We then discuss the potential mechanisms underlying hyperactivation in the context of Alzheimer's disease and provide a testable framework bridging hyperactivation, ageing, cognition and the Alzheimer's disease pathological cascade. We conclude with a discussion of future challenges and opportunities to advance our understanding of the fundamental disease mechanisms of Alzheimer's disease, and the promising development of therapeutic interventions incorporating or aimed at hyperactivation and large-scale functional systems.

Dataset Information

The Neuroinflammasome in Alzheimer's Disease and Cerebral Stroke.

Aim/background

Methods

Results

Conclusions

Publications

The Neuroinflammasome in Alzheimer's Disease and Cerebral Stroke.

Similar Datasets

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