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Therapeutic Efficacy of the Inositol D-Pinitol as a Multi-Faceted Disease Modifier in the 5×FAD Humanized Mouse Model of Alzheimer's Amyloidosis.
Nutrients
December 2024
Grupo de Neuropsicofarmacología, Instituto de Investigación Biomédica de Málaga y Plataforma en Nanomedicina-IBIMA Plataforma BIONAND, Unidades Clínicas de Neurología y Salud Mental, 29010 Málaga, Spain.
Background/objectives: Alzheimer's disease (AD), a leading cause of dementia, lacks effective long-term treatments. Current therapies offer temporary relief or fail to halt its progression and are often inaccessible due to cost. AD involves multiple pathological processes, including amyloid beta (Aβ) deposition, insulin resistance, tau protein hyperphosphorylation, and systemic inflammation accelerated by gut microbiota dysbiosis originating from a leaky gut.
View Article and Find Full Text PDFRole of Flavonoids in Mitigating the Pathological Complexities and Treatment Hurdles in Alzheimer's Disease.
Phytother Res
December 2024
Department of Pharmacology, Central University of Punjab, Bathinda, India.
With the passage of time, people step toward old age and become more prone to several diseases associated with the age. One such is Alzheimer's disease (AD) which results into neuronal damage and dementia with the progression of age. The existing therapeutics has been hindered by various enkindles like less eminent between remote populations, affordability issues and toxicity profiles.
View Article and Find Full Text PDFDoes Metabolic Manager Show Encouraging Outcomes in Alzheimer's?: Challenges and Opportunity for Protein Tyrosine Phosphatase 1b Inhibitors.
Drug Dev Res
December 2024
Department of Pharmacy, Banasthali Vidyapith, Banasthali, Rajasthan, India.
Protein tyrosine phosphatase 1b (PTP1b) is a member of the protein tyrosine phosphatase (PTP) enzyme group and encoded as PTP1N gene. Studies have evidenced an overexpression of the PTP1b enzyme in metabolic syndrome, anxiety, schizophrenia, neurodegeneration, and neuroinflammation. PTP1b inhibitor negatively regulates insulin and leptin pathways and has been explored as an antidiabetic agent in various clinical trials.
View Article and Find Full Text PDFIntranasal long R3 insulin-like growth factor-1 treatment promotes amyloid plaque remodeling in cerebral cortex but fails to preserve cognitive function in male 5XFAD mice.
J Alzheimers Dis
January 2025
Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY, USA.
Background: Insulin-like growth factor-1 (IGF-1) promotes neurogenesis, cell survival, and glial function, making it a promising candidate therapy in Alzheimer's disease (AD).
Objective: Long arginine 3-IGF-1 (LR3-IGF-1) is a potent IGF-1 analogue. We sought to determine whether intranasal (IN) LR3 treatment would delay cognitive decline and pathology in 5XFAD mice.
TREM2 bridges microglia and extracellular microenvironment: Mechanistic landscape and therapeutical prospects on Alzheimer's disease.
Ageing Res Rev
January 2025
Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China; Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, China. Electronic address:
Neuroinflammation is closely related to the pathogenesis of Alzheimer's disease (AD). One of its prominent cellular components, microglia, is a potent coordinator of neuroinflammation in interplay with the characteristic AD pathological alterations including Aβ, tau, and neuronal defects, which constitute the AD-unique extracellular microenvironment. Mounting evidence implicates Triggering Receptors Expressed on Myeloid Cells 2 (TREM2) in the center of microglial activation, a vital event in the pathogenesis of AD.
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