Publications by authors named "A Hatzimanolis"
Importance: Aging is accompanied by immune dysregulation, which has been implicated in Alzheimer's disease (AD) pathogenesis. Individuals who are genetically predisposed to elevated levels of proinflammatory mediators might be at increased risk for AD.
Objective: To investigate whether genetic propensity for higher circulating levels of interleukin 6 (IL-6) is associated with AD risk.
Article Synopsis
- Mild Behavioral Impairment (MBI) in older adults without dementia is associated with a higher risk of cognitive decline but lacks comprehensive understanding of its underlying causes.
- Research indicates MBI is linked to structural and functional changes in the brain, genetic risk factors for Alzheimer's disease, and various types of brain pathology involving amyloid and tau proteins.
- Potential mechanisms connecting MBI to these pathologies include disruptions in hormones, neurotrophic factors, neuroinflammation, and neurotransmitter balance, which could inform targeted treatment approaches and future research.
The tryptophan-metabolizing kynurenine pathway (KP) can be activated by enhanced inflammatory responses and has been implicated in the pathophysiology of schizophrenia. However, there is little evidence for KP dysregulation in the early course of psychotic illness. We aimed to investigate the potential immune-mediated hyperactivity of KP in individuals with first-episode psychosis (FEP) and the relationship with symptom severity and treatment response outcomes.
View Article and Find Full Text PDFThe possible relationship between Subjective Cognitive Decline (SCD) and dementia needs further investigation. In the present study, we explored the association between specific biomarkers of Alzheimer's Disease (AD), amyloid-beta 42 (Aβ) and Tau with the odds of SCD using data from two ongoing studies. In total, 849 cognitively normal (CN) individuals were included in our analyses.
View Article and Find Full Text PDFOur study aimed to explore whether physical condition might affect the association between genetic predisposition for Alzheimer's Disease (AD) and AD incidence. The sample of participants consisted of 561 community-dwelling adults over 64 years old, without baseline dementia (508 cognitively normal and 53 with mild cognitive impairment), deriving from the HELIAD, an ongoing longitudinal study with follow-up evaluations every 3 years. Physical condition was assessed at baseline through walking time (WT), while a Polygenic Risk Score for late onset AD (PRS-AD) was used to estimate genetic predisposition.
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