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In contrast to chronological aging, physical aging, which is more important for health and aging-related disorders, may differ between individuals. Aging, which is eventually associated with progressive physical deterioration and increased vulnerability to death, cannot be avoided. Despite the use of various antibodies to treat AD, there are still many unmet medical needs.Īging is an inevitable and definite risk factor for AD, which may accelerate aging. For example, aducanumab was approved by the Food and Drug Administration in the United States in June 2021, although its efficacy remains controversial. Antibodies against amyloid beta (Aβ) have been under clinical trials and have given us hope. Although there have been many studies on the development of AD treatment, there is no definitive cure, except for symptomatic treatment with donepezil, rivastigmine, galantamine, and memantine. AD is a major burden for aging societies worldwide, and its treatment should be established as soon as possible for the future of humans. We suggest that GV1001 exerts anti-ageing effects in 3xTg-AD mice by reducing neurodegeneration and senescence, which contributes to improved survival.Īlzheimer’s disease (AD) is one of the most critical neurodegenerative disorders, as elderly people over 65 years of age are increasing worldwide. It decreased BACE and Aβ 1-42 levels, neurodegeneration (i.e., reduced CA1, CA3 and dentate gyrus volume, decreased levels of senescence-associated β-galactosidase positive cells, and increased telomere length and telomerase activity), and levels of ageing-associated proteins. GV1001 increased the survival of 3xTg-AD mice. GV1001 crossed the blood-brain barrier, as confirmed by assessing the status of ferrocenecarboxylic acid-conjugated GV1001 using magnetic resonance imaging and PBS. Diverse molecular studies were performed to investigate the effect of GV1001 on neurodegeneration and cellular senescence in AD model mice, with a particular focus on BACE, amyloid beta 1-42 (Aβ 1-42), phosphorylated tau, volume of dentate gyrus, β-galactosidase positive cells, telomere length, telomerase activity, and ageing-associated proteins. Magnetic resonance imaging (MRI) and Prussian blue staining (PBS) were performed to evaluate entry of GV1001 entrance into the brain. GV1001 (1 mg/kg) was subcutaneously injected into old 3xTg-AD mice thrice a week until the endpoint for sacrifice, and survival was analysed. This study aimed to investigate the effects of GV1001 on neurodegeneration, senescence, and survival in triple transgenic Alzheimer’s disease (3xTg-AD) mice. However, the underlying protective mechanisms remain unclear. As per a recent phase II clinical trial, it improves cognitive function in patients with moderate to severe dementia.
GV1001, which mimics the activity of human telomerase reverse transcriptase, protects neural cells from amyloid beta (Aβ) toxicity and other stressors through extra-telomeric function, as noted in our prior in vitro studies.