Cells, Journal Year: 2024, Volume and Issue: 13(16), P. 1388 - 1388
Published: Aug. 20, 2024
This Special Issue of Cells presents a collection 22 published, peer-reviewed articles on the theme “Astrocytes in CNS Disorders,” including 9 reviews evidence implicating astrocytes etiology specific disorders, and 13 original research papers providing such [...]
Language: Английский
Neuroscience & Biobehavioral Reviews, Journal Year: 2024, Volume and Issue: 162, P. 105724 - 105724
Published: May 16, 2024
Alzheimer's disease (AD) is prevalent around the world, yet our understanding of still very limited. Recent work suggests that cornerstone AD may include inflammation accompanies it. Failure a normal pro-inflammatory immune response to resolve lead persistent central contributes unsuccessful clearance amyloid-beta plaques as they form, neuronal death, and ultimately cognitive decline. Individual metabolic, dietary (lipid) profiles can differentially regulate this inflammatory process with aging, obesity, poor diet, early life stress other factors contributing greater risk developing AD. Here, we integrate evidence for interface between these factors, how contribute brain milieu. In particular, discuss importance appropriate polyunsaturated fatty acids (PUFA) in diet metabolism specialised pro-resolving mediators (SPMs); raising possibility strategies improve outlook.
Language: Английский
Citations
5
BioMed, Journal Year: 2025, Volume and Issue: 5(1), P. 3 - 3
Published: Jan. 9, 2025
Background: Alzheimer’s disease (AD), the leading cause of dementia worldwide, poses an increasing global health burden, yet its pathogenesis remains poorly understood. Diabetes mellitus (DM), characterized by chronic hyperglycemia, has been identified as a significant risk factor for AD development, suggesting potential metabolic and molecular link between these diseases. Methods: This study examines impact sustained high glucose levels on astrocyte-like C6 glial cells, focusing key cellular processes associated with AD. We evaluated mitochondrial function, oxidative stress, uptake, expression hallmark proteins, including β-amyloid hyperphosphorylated tau. Results: Our findings demonstrate that exposure triggers hyperactivity, increased Tau phosphorylation, though were unaffected within experimental timeframe. Conclusions: These results shed light early dysfunctions contributing to DM-AD connection, providing valuable insights into pathways involved identifying therapeutic targets mitigate progression in individuals DM.
Language: Английский
Citations
0
Brain Behavior and Immunity, Journal Year: 2025, Volume and Issue: 126, P. 80 - 97
Published: Feb. 5, 2025
Language: Английский
Citations
0
Alzheimer s & Dementia, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 12, 2025
Abstract BACKGROUND Despite significant astrocytic involvement in Parkinson's disease (PD), the knowledge regarding role of reactive astrogliosis is still at surface level; largely due to lack specific biomarkers track these processes. Novel astroglial PET‐tracers BU99008 and Deprenyl, hold immense potential for visualizing PD. However, they have not been thoroughly investigated METHODS We employed a multi‐marker approach performed vitro radioligand binding autoradiography studies with 3 H‐BU99008 H‐Deprenyl together immunofluorescence morphometric analyses frontal cortex, temporal caudate putamen brain regions PD ( n = 4) control 7) cases. RESULTS AND DISCUSSION showed distinct behavior displayed diverse array sites (single or multiple) brains. Importantly, captured pronounced regions, corroborated by marked changes markers, morphology, cellular Highlights Astroglial tracers Deprenyl range different levels affinity proportions (%) healthy (CN) (PD) highly (permanent) high‐affinity (HA) site nanomolar range, which might be consistent across pathologies. highlighted tracer behavior, indicating that targeting subpopulations states astrocytes CN prominent advanced/end stages PD, substantiated increase intercellular adhesion molecule 1 (ICAM‐1)–positive morphology
Language: Английский
Citations
0
International Immunopharmacology, Journal Year: 2024, Volume and Issue: 141, P. 112940 - 112940
Published: Aug. 17, 2024
Language: Английский
Citations
3
Journal of Neurochemistry, Journal Year: 2024, Volume and Issue: unknown
Published: Sept. 17, 2024
Abstract Glial fibrillary acidic protein (GFAP) is a well‐established biomarker of reactive astrogliosis in the central nervous system because its elevated levels following brain injury and various neurological disorders. The advent ultra‐sensitive methods for measuring low‐abundant proteins has significantly enhanced our understanding GFAP serum or plasma patients with diverse diseases. Clinical studies have demonstrated that holds promise both as diagnostic prognostic biomarker, including but not limited to individuals Alzheimer's disease. exhibits forms structures, herein referred proteoform complexity, encompassing conformational dynamics, isoforms post‐translational modifications (PTMs). In this review, we explore how complexity influences detection, which may affect differential performance different biological fluids can provide valuable insights into underlying processes. Additionally, proteoforms are often disease‐specific, review provides suggestions highlights areas focus on development new assays GFAP, isoforms, PTMs, discharge mechanisms, breakdown products, higher‐order species interacting partners. By addressing knowledge gaps highlighted aim support clinical translation interpretation CSF blood reliable, reproducible specific tests. To enhance disease pathology comprehension optimise thorough detected biofluids essential. image
Language: Английский
Citations
3
Methods in molecular biology, Journal Year: 2024, Volume and Issue: unknown, P. 195 - 218
Published: Jan. 1, 2024
Language: Английский
Citations
2
Metabolic Brain Disease, Journal Year: 2024, Volume and Issue: 39(6), P. 1231 - 1254
Published: July 24, 2024
Language: Английский
Citations
2
Cellular and Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 44(1)
Published: Oct. 23, 2024
The neurotoxicant trimethyltin (TMT) triggers cognitive impairment and hippocampal neurodegeneration. TMT is a useful research tool for the study of Alzheimer's disease (AD) pathogenesis treatment. Although antidiabetic agent metformin has shown promising neuroprotective effects, however, its precise modes action in neurodegenerative disorders need to be further elucidated. In this study, we investigated whether can mitigate cognition To induce an AD-like phenotype, was injected i.p. (8 mg/kg) administered daily p.o. 3 weeks at 200 mg/kg. Our results showed that administration group mitigated learning memory Barnes maze, novel object recognition (NOR) task, Y attenuated oxidative, inflammatory, cell death/pyroptotic factors, also reversed neurodegeneration-related proteins such as presenilin 1 p-Tau. Hippocampal level AMP-activated protein kinase (AMPK) key regulator energy homeostasis improved following Additionally, reduced acetylcholinesterase (AChE) activity, glial fibrillary acidic (GFAP)-positive reactivity, prevented loss CA1 pyramidal neurons. This TMT-induced neurodegeneration may pave way develop new therapeutics combat against deficits under neurotoxic conditions.
Language: Английский
Citations
2
Journal of Alzheimer s Disease, Journal Year: 2024, Volume and Issue: 100(3), P. 1017 - 1037
Published: July 12, 2024
Alzheimer's disease (AD) is the most common neurodegenerative disease. Unfortunately, efficient and affordable treatments are still lacking for this disorder, it therefore urgent to identify new pharmacological targets. Astrocytes playing a crucial role in tuning of synaptic transmission several studies have pointed out severe astrocyte reactivity AD. Reactive astrocytes show altered physiology function, suggesting they could early pathophysiology
Language: Английский
Citations
1