Publications by authors named "N C Krishnadas"
Article Synopsis
- Plasma phospho-tau 217 (pTau217) assays, when performed on the common Lumipulse-G® platform, can effectively identify Alzheimer's disease (AD) by analyzing β-amyloid (Aβ) status and tau staging in patients.
- In a study with 388 participants, pTau217 showed strong correlations with PET imaging results, achieving high accuracy rates in distinguishing between Aβ-negative and Aβ-positive individuals, as well as different stages of tau pathology.
- The findings suggest that the plasma pTau217 assay is a reliable tool for predicting who might benefit from anti-β-amyloid treatments, emphasizing its potential for broader clinical use in AD diagnostics.
Article Synopsis
- The study examines the types of diagnoses given to patients referred for frontal network impairments at a cognitive neurology clinic in Melbourne, specifically looking into cases suspected of frontotemporal dementia (FTD).
- Out of 161 patients analyzed over a decade, the most common final diagnosis was an FTD syndrome, with behavioral variant FTD being the most frequent sub-type.
- Other diagnoses included primary psychiatric disorders, vascular cognitive impairment, and Alzheimer's disease, with behavioral variant FTD patients showing higher rates of medical comorbidities.
Sickness behaviour, a set of behavioural changes associated with neuroinflammation, is expressed as decreased mobility and depressed behaviour. Activation of AMP-activated protein kinase (AMPK) is reported to regulate inflammation in conditions such as Alzheimer and traumatic brain injury. Metformin, an antidiabetic agent acting via AMPK activation, possesses anti-inflammatory properties.
View Article and Find Full Text PDFBlood biomarkers are an emerging diagnostic and prognostic tool that reflect a range of neuropathological processes following traumatic brain injury (TBI). Their effectiveness in identifying long-term neuropathological processes after TBI is unclear. Studying biomarkers in the chronic phase is vital because elevated levels in TBI might result from distinct neuropathological mechanisms during acute and chronic phases.
View Article and Find Full Text PDF