Acta Neuropathol: Gene new therapy beats you to reverse Alzheimer's-related memory loss.

Today, Alzheimer's disease (AD) is a global public health and social problem.
data show that every three seconds, there is one more AD patient in the world.
the total number of AD patients worldwide will exceed 50 million by 2018, and that number is expected to exceed 150 million by 2050.
early stages, AD is characterized by the accumulation and memory loss of amyloid (A beta) and tau proteins in the brain.
, however, the current therapeutic effect of targeting beta-amyloid proteins or processing amyloid prey proteins (APP) is not ideal.
, scientists focused their exploration of disease pathology and therapeutic development on tau protein.
July 29
A study by the brothers, Arne Ittner and Professor Lars Ittner of the Dementia Research Centre at Macquarie University in Sydney, Australia, showed that the active form of tau kinase p38 to neurons could improve the cognition of mice with AD models that already had significant memory impairments.
the study was published in Acta Neuropathologica.
's team has previously shown that by introducing genetic material into the cells of sick mice, tau kinase p38 can be activated to prevent the development of Alzheimer's disease, and their latest study is based on this.
, in this study, the researchers aimed to determine whether increasing the activity of neuron p38 gamma has the potential to improve the treatment of existing memory impairments.
they found that by increasing the activity of the synaptic kinase p38, which targets T205 in tau, memory defects in symptomatic A-beta-induced AD models were reduced.
Subsequently, the researchers reconstructed the Tau T205A with wild human tau protein or phosphorylation defects, and the results showed that T205 modification was essential for the downstream effect of p38, which prevented memory damage in APP genetically modified mice.
addition, gene editing of T205 cotons in the Mapt gene in mice showed that the one-sided chain of endogenic tau protein was the key to regulating memory deficiency in mice with genetically modified APP Alzheimer's disease.
The researchers also found that in genetically modified mouse models that did not express human pathogenic tau proteins, the protective effect of p38 was eliminated by the absence of the p38 gamma gene, which was toxic and led to impaired memory function in the absence of human A-beta.
results of these studies suggest that regulating p38 gamma activity can be used as an intrinsic tau protein-dependent treatment to improve cognitive impairment in advanced Alzheimer's disease.
the authors say the gene therapy may be used to treat other forms of dementia, such as frontal lobe dementia, which usually affects young people.
study found that there were no adverse events in mice, even when receiving high doses for long periods of time, so the team is planning to trial the therapy in humans.
has been conducting basic research for decades to understand the causes of Alzheimer's disease, and if the treatment works in clinical trials, it would be good news for thousands of Alzheimer's patients.
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