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Background: Alzheimer's disease (AD), a hallmark of age-related cognitive decline, is defined by its unique neuropathology. Metabolic dysregulation, particularly involving glutamine (Gln) metabolism, has emerged as a critical but underexplored aspect of AD pathophysiology, representing a significant gap in our current understanding of the disease.

Methods: To investigate the involvement of GlnMgs in AD, we conducted a comprehensive bioinformatic analysis.

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Alzheimer's disease (AD) is a prominent neurodegenerative disorder affecting the central nervous system in the elderly. Current understanding of AD primarily centers on the gradual decline in cognitive and memory functions, believed to be influenced by factors including mitochondrial dysfunction, β-amyloid aggregation, and neuroinflammation. Emerging research indicates that neuroinflammation plays a significant role in the development of AD, with the inflammasome potentially mediating inflammatory responses that contribute to neurodegeneration.

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Alzheimer's disease (AD), a progressive neurodegenerative disorder, is frequently associated with musculoskeletal complications, including sarcopenia and osteoporosis, which substantially impair patient quality of life. Despite these clinical observations, the molecular mechanisms linking AD to bone loss remain insufficiently explored. In this study, we examined the femoral bone microarchitecture and transcriptomic profiles of APP/PS1 transgenic mouse models of AD to elucidate the disease's impact on bone pathology and identify potential gene candidates associated with bone deterioration.

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Studies of the genetics of Alzheimer's disease (AD) have largely focused on single nucleotide variants and short insertions/deletions. However, most of the disease heritability has yet to be uncovered, suggesting that there is substantial genetic risk conferred by other forms of genetic variation. There are over one million short tandem repeats (STRs) in the genome, and their link to AD risk has not been assessed.

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Background: Osteoarthritis is associated with a higher risk of developing dementia, though the underlying biological mechanisms have remained unclear. Recent studies suggest that blood phosphorylated tau proteins, particularly Tau-PT217, are sensitive biomarkers capable of detecting cognitive decline in its early stages, making it useful for early diagnosis of Alzheimer's disease and other forms of cognitive impairment.

Methods: In this study, we investigated the plasma phosphorylated tau protein levels (Tau-PT217 and Tau-PT181), hippocampus functional connectivity, and cognitive function in people with knee osteoarthritis compared to age and gender matched pain-free controls.

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