早期诊断阿尔茨海默氏症：生物标志物的突破

By Alexandra Sommer

The race to find a way of spotting and treating Alzheimers at an early stage is heating up but there’s a long way still to go. Or is there?

According to the World Health Organization (WHO), people aged 60 and over will account for 22% of the world’s population by 2050.1 The fact that we’re living long than ever before is, of course, something to celebrate. But with longevity comes a whole other set of challenges. One of these is what to do about Alzheimer’s.

Advancing age is the greatest risk factor

Dedicated to advancing Alzheimer’s research worldwide, alz.org says that it’s already the most expensive disease in the US and the only one currently without a way to ‘prevent, cure or even slow its progression’. Because Americans are living longer, numbers of Alzheimer’s sufferers are predicted to soar to as many as 16 million by 2050, ‘costing the nation $20 trillion over the next 40 years’.

If a treatment that delays the onset of Alzheimer’s by five years was introduced in 2025, alz.org calculates, it would reduce the number of people affected by 2.5 million. And, it would save the US $220 billion within the first five years of a treatment being made available.

A World Health Organization (WHO) paper estimated that the number of people with dementia worldwide in 2010 was 35.6 million.1  By 2050 this is expected to rise to 115.4 million in 2050. The total number of cases worldwide each year is nearly 7.7 million – one case every four seconds.

So, the race is well and truly on to find a cure for Alzheimer’s

What causes Alzheimer’s?

Although scientists are not yet sure what causes Alzheimer’s in most people, it’s agreed that a genetic mutation is usually the cause of the early-onset of the disease. According to the U.S. National Institute on Aging, ‘Late-onset Alzheimer’s arises from a complex series of brain changes that occur over decades. The causes probably include some combination of genetic, environmental and lifestyle factors.’2

Research on normal brain ageing is beginning to shed light on why it mainly strikes older people, with symptoms becoming apparent in their mid-60s. The apolipoprotein E (APOE) gene is involved and one of them is APOE ε4. This increases a person’s chance of developing the disease but people who don’t carry APOE ε4 may also end up with Alzheimer’s. The possible relationship between cognitive decline and conditions like heart disease, stroke, high blood pressure, diabetes and obesity is also being explored.

This, inevitably, has led to the question of whether a change in lifestyle, including diet, might make a difference. For instance, the MIND diet, rich in vegetables, berries, whole grains and nuts, lowered the risk by ‘as much as 53 per cent in participants who adhered to the diet rigorously’.

Of course, this is exciting news. But the study was carried out on people who changed their diet after they’d had a stroke. The question of how to early diagnose people who are at risk of developing Alzheimer’s still remains.

这是关于早期诊断

IBL International的Oliver Schmidt是一家生产可帮助研究人员研究阿尔茨海默氏症的试剂盒的公司，他说，问题在于大脑萎缩和标志性蛋白沉积 - 淀粉样蛋白斑和tau原纤维 - 只能在死后脑检查中明确发现。 阿尔茨海默病的药物将在很多年前，远在疾病特征的认知障碍已经显现之前就开始服用。

正如国家脑研究中心的Pravat K Mandala所说，这就是迫切需要开发可在早期阶段检测AD病理的可靠诊断生物标志物。 这些生物标志物不仅有助于早期检测，还将为有效的临床试验铺平道路.

生物标志物的突破

2014年7月在FierceDiagnostics.com上发布的一则报道称，英国研究人员已经在血液中发现了10种蛋白质生物标志物，这些标志物可能有助于预测阿尔茨海默氏症的发病。这在阿尔茨海默氏症的诊断和治疗疾病方面实现了巨大的飞跃。

进行这项研究的国王学院/蛋白质组学认为，基于其生物标志物的血液测试远比PET脑部扫描和腰椎液中的血浆更简单。

今年早些时候，药物制造商Biogen和Eli Lilly发布了他们的计划更新，以开发清除大脑中淀粉样蛋白斑块积聚的药物，并减缓阿尔茨海默氏症的认知下降。这两种药物都显示出能够做到他们说的话，但似乎还有很长的路要走。

但是，另一项研究还认为研究人员需要敞开心扉，摆脱“淀粉样蛋白级联假说”，这种假设限制了生物标志物和药物开发的范围。

期待

尽早找到一种诊断阿尔茨海默氏症的方法显然会使制药公司受益匪浅。 但最大的赢家将是数百万人和那些关心他们的人，否则他们将遭受极大的痛苦。

我们根本不能让阿尔茨海默氏症的情况持续更长时间。 我们能期待阿尔茨海默病只是记忆的那一天吗？

老年痴呆检测相关试剂盒

代理商：深圳市科润达生物工程有限公司

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