New perspective on neurodegeneration: the role of the neurochemical T14 in Alzheimer's disease
最近審查：14.06.2024
所有iLive內容都經過醫學審查或事實檢查，以確保盡可能多的事實準確性。
我們有嚴格的採購指南，只鏈接到信譽良好的媒體網站，學術研究機構，並儘可能與醫學同行評審的研究相關聯。 請注意括號中的數字（[1]，[2]等）是這些研究的可點擊鏈接。
如果您認為我們的任何內容不准確，已過時或有疑問，請選擇它並按Ctrl + Enter。
An international team of clinicians and neuroscientists has published a new review of the process of neurodegeneration. Their findings examine the mechanism that precedes amyloid formation, including a key neurochemical factor that contributes to this process.
The paper, published in Alzheimer's & Dementia, focuses on the isodendritic nuclei, a group of neurons distinct from the rest of the brain and previously identified as being primarily vulnerable to
Alzheimer's disease (AD).
The authors acknowledge that amyloid is a significant factor in late-stage AD, but note that it is absent from these early-stage neurons. If damage occurs to these vulnerable neurons in adulthood, they respond by mobilizing a response mechanism. This mechanism typically promotes neuronal growth during embryonic and early life, but is detrimental in adulthood.
The review describes how the key molecule driving this process is the bioactive 14-mer peptide T14, which selectively activates one target receptor. In the mature brain, instead of restoring normal function, T14 causes neuronal death and initiates a negative snowball effect that grows stronger over time.
Isodendritic nuclei, located deep in the brain, are responsible for arousal and sleep/wake cycles and are not directly linked to higher functions such as memory. Thus, the degeneration process can continue without obvious symptoms until damage spreads to areas responsible for cognition.
The proposed explanation in the paper may explain the long delay of 10-20 years from the onset of neuronal loss to the onset of cognitive impairment.
The review reports that T14 can be detected at a very early stage of AD, which may serve as a presymptomatic indication of the onset of neurodegeneration and thus could be developed as a biomarker.
In addition, the authors describe how a cyclized version of T14, NBP14, can block the action of T14. NBP14 has been shown to prevent memory impairment in a mouse model of AD, and its mechanism of action has been demonstrated in various studies, including postmortem studies of human brain tissue. Thus, NBP14 may become the basis for a new therapeutic strategy.
This new approach offers important discoveries that could significantly impact the early diagnosis and treatment of Alzheimer's disease, highlighting the importance of further research in this area.