As the number one cause of dementia, Alzheimer's disease (AD) affects millions of people worldwide. AD was first described in 1907, but until now treatment is still limited to drugs that only reduce symptoms, such as donepezil, galantamine, rivastigmine, and memantine. The two hallmarks of AD are the extracellular neuritic plaque, which mainly composed of the amyloid-beta peptide, and the intracellular neurofibrillary tangle, which is made up of a different protein called tau. Some studies suggest these neuritic plaques and neurofibrillary tangles damage nerve cells in the brain, resulting in impairment of certain brain functions. But other studies indicate that people with high amyloid levels may show no symptoms of AD. More research is required to better understand the pathogenesis of the disease.
Now a study in the latest edition of eLife has demonstrated that low levels of the protein NPTX2 in the brain are associated with cognitive decline in individuals with AD. The study is led by Paul Worley at Johns Hopkins University School of Medicine.
Memory loss in AD is caused by pervasive weakening and loss of synapses. In this work, Worley and colleagues conducted a series of experiments in human brain tissue samples and genetically engineered mice. Western blot analysis showed that the protein NPTX2 in brains from patients with late onset AD was lower than that in age-matched controls. The researchers also found that when NPTX2 is turn down and amyloid accumulates in the brain, circuit adaptations crucial for neurons are disrupted, leading to a failure of memory. (Cusabio offers NPTX2 and Recombinant RHO proteins.)
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