研究人员成功逆转小鼠中的阿尔茨海默病:同行评审研究
Researchers Successfully Reverse Alzheimer's In Mice: Peer-Reviewed Study

原始链接: https://www.zerohedge.com/medical/researchers-successfully-reverse-alzheimers-mice-peer-reviewed-study

发表在《细胞报告·医学》上的一项最新研究,在阿尔茨海默病研究中取得了一项令人鼓舞的突破,展示了在小鼠身上逆转该疾病的可能性。研究人员使用一种名为P7C3-A20的药物,对携带淀粉样蛋白或tau蛋白突变的小鼠进行治疗——这两者都是阿尔茨海默病的关键因素。 该治疗恢复了健康的NAD+水平,这是一种至关重要的细胞能量分子,会随着年龄增长而下降,并与阿尔茨海默病的进展有关。这种恢复导致了多个方面的改善:血脑屏障恶化的逆转、DNA损伤和神经炎症的减少,以及突触可塑性和神经元生成的增强。 值得注意的是,接受P7C3-A20治疗的小鼠经历了完全的认知恢复,并且关键阿尔茨海默病生物标志物的水平降低。即使在患有晚期疾病的小鼠中,6个月的治疗在12个月内也带来了全面的大脑健康恢复。研究人员认为,这些发现挑战了阿尔茨海默病不可逆转的观念,并强调了NAD+平衡作为潜在的治疗靶点。虽然研究作者拥有相关专利,但这些发现令人鼓舞,并值得在人类中进行进一步的临床试验。

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原文

Authored by Naveen Athrappully via The Epoch Times (emphasis ours),

Scientists have reversed Alzheimer’s disease in mice, potentially showing a pathway to treat the illness among humans, according to a Dec. 22 peer-reviewed study published in the Cell Reports Medicine journal.

A nurse holds the hands of a person suffering from Alzheimer's disease at Les Fontaines retirement home in Lutterbach, France, on Sept. 21, 2009. Sebastien Bozon /AFP via Getty Images

Alzheimer’s is traditionally considered irreversible. In the study, researchers treated two groups of mice with P7C3-A20, a pharmacologic agent. One group carried human mutations related to amyloid processing, while the other carried a tau protein mutation. Both amyloid and tau pathologies are two major early events of Alzheimer’s.

Researchers say that as mice develop brain pathologies resembling Alzheimer’s, they are ideal subjects to test how P7C3-A20 affects Alzheimer’s in humans.

Among the amyloid mice, treatment with P7C3-A20 was found to have resulted in restoring the proper balance of Nicotinamide adenine dinucleotide (NAD+), which is a cellular energy molecule and a major driver of Alzheimer’s disease. As people age, NAD+ levels decline in their bodies, including the brain. Without proper NAD+ balance, the cells are unable to execute critical processes necessary for proper functioning.

The treatment was found to have reversed blood-brain barrier deterioration, DNA damage, oxidative stress, and neuroinflammation, researchers wrote. The blood-brain barrier maintains nutrient and hormone levels in the brain while protecting the organ from toxins and pathogens.

The treatment enhanced synaptic plasticity and hippocampal neurogenesis, a process in which new functional neurons are generated.

These changes resulted in “full cognitive recovery and reduction of plasma levels” of p-tau217 among the amyloid mice, researchers said. P-tau217 is the clinical biomarker of Alzheimer’s that helps predict cognitive decline.

In fact, when P7C3-A20 was initiated for 6-month-old mice as they manifested advanced Alzheimer’s pathology and cognitive deficits, the treatment “comprehensively restored brain health and function by 12 months,” researchers wrote in the study.

P7C3-A20 reversed advanced Alzheimer’s in mice with tau mutation and was found to help protect the human brain microvascular endothelial cells (BMEC) from oxidative stress. BMEC is the major component of the blood-brain barrier.

“Our results challenge the long-held view that [Alzheimer’s disease] is intrinsically irreversible,” the researchers wrote.

They said that restoring the proper balance of NAD+ levels may be “a potentially transformative therapeutic approach.”

Multiple study authors declared competing interests for holding patents related to subjects covered under the study.

In a Dec. 22 statement, Ohio-based University Hospitals, whose researchers took part in the study, said the findings should spark new research into complementary approaches and clinical testing in Alzheimer’s patients.

Andrew A. Pieper, senior author of the study, said that they were “very excited and encouraged” by the results.

“The key takeaway is a message of hope—the effects of Alzheimer’s disease may not be inevitably permanent,” he said. “The damaged brain can, under some conditions, repair itself and regain function.”

Alzheimer’s is a progressive illness that starts with mild memory loss and eventually leads to a situation where the person is unable to carry on conversations or conduct daily activities.

Alzheimer’s typically affects people aged 60 and older. While the exact causes of the illness remain unknown, Alzheimer’s is likely the result of various factors such as genes, environment, family history, and lifestyle behaviors, according to an August 2024 report from the Centers for Disease Control and Prevention.

An October 2024 study identified that a silent phase of Alzheimer’s begins up to 20 years before symptoms appear.

This silent phase is marked by subtle changes in brain cells. For instance, the inhibitory neurons could become vulnerable, thus disrupting communication between brain cells. In this phase, there is a gradual buildup of beta-amyloid plaques and tangles, which are hallmarks of Alzheimer’s.

According to data from the nonprofit Alzheimer’s Association, more than 7 million Americans currently live with the illness, a number projected to jump to almost 13 million by 2050.

About one in nine individuals aged 65 and older has Alzheimer’s. Almost 12 million Americans are estimated to provide unpaid care for people with Alzheimer’s or other types of dementia, valued at more than $413 billion last year.

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