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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by hallmark pathologies that affect many brain regions, including the cellular microenvironment with the hippocampus, ultimately leading to profound deficits in cognition. Surprising recent work has shown that factors in the systemic environment regulate the hippocampal cellular niche; age-associated blood-borne factors exacerbate brain aging phenotypes, whereas youth-associated blood-borne factors, including tissue inhibitor of metalloproteinases 2 (TIMP2), reverse or ameliorate features of brain aging. As aging serves as the major risk factor for AD, and recent work shows that systemic factors can regulate AD pathology, we sought to characterize mechanisms by which the systemic environment regulates CNS phenotypes relevant to AD pathology through changes in neuroinflammation.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
The University of Queensland, Brisbane, QLD, Australia.
Ageing changes the adult brain at the molecular, cellular and functional levels, driving regenerative decline, inflammation, cognitive impairments and susceptibility to dementia-related neurodegenerative disorders, such as Alzheimer's disease (AD). There is overwhelming evidence that regular physical exercise can counteract cognitive decline in both healthy ageing and in neurodegenerative conditions such as AD, with exerkines, the circulating humoral factors that are secreted into the blood stream in response to exercise, emerging as likely mediators of this response. However, the source and identity of these exerkines remain unclear.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Brown University, Providence, RI, USA.
Background: Chitinase-3-like protein 1 (CHI3L1, or YKL-40) is an important regulator of immunity and, in the brain, is primarily secreted by activated astrocytes and heralds a neurotoxic inflammatory state. While it has been well known as a high-profile biomarker for Alzheimer's disease (AD) and inflammatory brain conditions (e.g.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Background: Excessive high-fat diet (HFD) consumption develops the obese pre-diabetic condition, which initiates neuroinflammation and numerous brain pathologies, resulting in cognitive decline (1). A cinnamamide derivative compound (2i-10) is recently identified as a novel myeloid differentiation factor 2 (MD-2) inhibitor, and has been shown to attenuate inflammation via toll-like receptor 4 (TLR4) signaling pathway (2). However, the effects of 2i-10 on the neuroinflammation, brain pathologies and cognitive function in the obese pre-diabetic rats have never been studied.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: The apolipoprotein E (APOE) ε4 allele is the strongest genetic risk factor for Alzheimer's disease (AD), increasing risk from 3-12-fold relative to the common ε3 allele. Seminal studies have revealed that age-related changes in blood-CNS communication regulate cognitive function. More recently, youth-associated blood-borne proteins revitalize the aged brain, improving hippocampal function and increasing adult neurogenesis and dendritic spine plasticity.
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