Tau，β淀粉样蛋白和深部脑刺激：旨在恢复阿尔茨海默氏症的认知功能障碍

Title:Tau, Amyloid Beta and Deep Brain Stimulation: Aiming to Restore Cognitive Deficit in Alzheimer's Disease

Volume: 14 Issue: 1

Author(s): Siddhartha Mondragón-Rodríguez, George Perry, Fernando Pena-Ortega, Sylvain Williams

Affiliation:

关键词: β-淀粉样蛋白，脑疾病，神经刺激，磷酸化，突触失效，突触可塑性，tau蛋白，治疗靶点

摘要: Background: The last two decades have seen a great advance in the data that supports the two current hypotheses in Alzheimer's disease field, the amyloid beta hypothesis and the tau hypothesis. Not surprisingly, Aβ and tau proteins are currently the major therapeutic research targets for AD treatment. Unfortunately, nothing but moderate success has emerged from such therapeutic approaches. With this in mind, we will discuss deep brain stimulation as a promising therapeutic strategy that aims to restore brain activity. Lastly, in the scope of cognitive deficit restoration, we will discuss the relevance of the limbic formation as a promising neuroanatomical target for deep brain stimulation.

Methods: Immunohistochemistry for modified tau (phosphorylated at Ser199–202–Thr205 labelled by the antibody AT8) was performed on paraffin-embedded human brain sections providing a detailed characterization of NFT pathology.

Results: Abnormally phosphorylated tau protein is the key common marker in several brain diseases such as Alzheimer's disease, Parkinson's disease, Pick Disease, Down syndrome and frontotemporal dementia and is capable of affecting synaptic events that are critical for memory formation. With this in mind, therapeutic strategies aiming to restore synaptic events could offer better outcomes.

Conclusion: The humble success of current therapeutic strategies along with the lack of basic knowledge of the brain disease mechanisms calls for alternatives that benefit patients in the present moment. One of particular interest is the neurostimulation strategy that is already a well-established treatment for several movement disorders and when compared to current Alzheimer's therapeutic strategies, deep brain stimulation does not directly interfere with the normal protein function, therefore increasing the probability of success.

Cite this article as:

Siddhartha Mondragón-Rodríguez, George Perry, Fernando Pena-Ortega, Sylvain Williams , Tau, Amyloid Beta and Deep Brain Stimulation: Aiming to Restore Cognitive Deficit in Alzheimer's Disease, Current Alzheimer Research 2017; 14 (1) . https://dx.doi.org/10.2174/1567205013666160819131336

DOI https://dx.doi.org/10.2174/1567205013666160819131336	Print ISSN 1567-2050
Publisher Name Bentham Science Publisher	Online ISSN 1875-5828