Studies have shown that it can lead to nerve degeneration by causing oxidative stress, worsening amyloid toxicity, interfering with tau protein function, and promoting neuron cell death. The prospective study, which was recently published between January 2015 and November 2022, evaluated the method of predicting the cognitive decline of the participants without the mild cognitive impairment (MCI) and cognitive damage by evaluating the measured brain and amyloid -ß (Aß) levels using quantitative sensitivity mapping (QSM) MRI and PET (QSM) MRI and PET (N) (N) (N) = 158).
The high baseline self -sensitivity in the MRI, led by XU LI and PHD, researchers of FM KIRBY Research Center for functional brain images of Kennedy Krieger Institute, was associated with an increase in the risk of mild cognitive impairment. blood = .005) and PET sub -group (risk ratio, 3.59; blood <.001). In addition, higher baseline brain cortex (β = -0.022; blood = .008) and Putamen (β = -0.018; blood = .04) The sensitivity of the lower PET sub -group was especially related to the decrease in cognition of the world, especially with the amyloid pathological abnormalities.
Following the publication neurology We have followed Li to get further commentary on the importance of this discovery and the potential for using QSM MRI. In the discussion, LI provided clinical insights in the role of brain iron in cognitive decrease in individuals with amyloid pathology. He also emphasized the need for more targeted research in the brain region, which is sensitive to iron change, in -depth exploration of iron interaction with amyloid and tau, and QSM standardized efforts for the use of braoid clinical use.
Neurology: What is the motive and origin of this study?
Xu Li, PHD: We were motivated by the early and more practical biomarkers of Alzheimer’s disease. Amyloid -β and tau are well -established markers, but are generally detected by PET scans, which costs high and contains radiation. In contrast, MRI is widely available and safe, but traditional measures, such as brain atrophy, only capture the changes in neurochromatics in the late stage. In addition, the therapy that targeted amyloids only showed a humble effect and emphasized the importance of other common paths. As evidence increases that abnormal brain iron can play an important role in Alzheimer’s nerve degeneration, we wanted to test whether QSM, a MRI method that can accurately measure brain railroads, can act as an initial non -invasive marker of dementia risk a few years before a mild cognitive impairment occurs.
As a result, what is the biggest clinical takeout?
The main takeout is to predict who will occur in the memory -related areas such as the Entorhinal Cortex, the higher the brain iron levels, the minor cognitive impairment (MCI) and the transitional stage of dementia. In addition, high brain iron is especially associated with faster overall cognitive reduction over time in individuals with amyloid pathology.
Clinically, this suggests that PET video can be supplemented by strengthening the important role of brain iron in the Alzheimer’s nerve degeneration and providing QSM safe and MRI -based biomarkers for early risk assessments. In addition, the brain iron itself increases the possibility of a therapeutic goal, but in this area, much more work is required.
Should there be more dedicated research on ENTORHINAL CORTEX and PUTAMEN? How can we target this in the right way?
yes. Entorhinal Cortex is one of the initial areas of Alzheimer’s Pathology, and Putamen seems to be sensitive to iron -related changes. Our findings emphasize the need for more targeted research in this area, which ideally combines QSM with other Alzheimer’s biomarkers such as amyloid and tau. As with technology development, longitudinal research is essential. For example, some groups are already developing high -resolution QSMs for areas such as hippocampus and enterhinal cortex, which can provide more sensitive measures and deeper insights to pathological changes that occur during Alzheimer’s disease.
How did the relationship between dialogue with Brain Iron and nerve degeneration evolved over the years? What questions should we still answer?
Interest in brain iron dates back to the 1950s. Later, senior steel was found in many neuromoduscular diseases, including Alzheimer’s. Damaged brain homeostasis, especially iron overload, is known to cause oxidation, cell damage and iron -related cell death. What has been changed recently is the same technology as the QSM MRI, which is the ability to accurately measure iron in vivo. In addition, the new evidence shows that iron can accelerate nerve degeneration through complex mechanisms by interacting with amyloid and tau.
In particular, the main question remains, whether iron is a causal and driver of the disease or a by -product of other processes. It is still not clear whether iron is an effective treatment that can correctly interact with amyloid and tau, and to modify these risks and slow cognitive reduction.
Should Brain Iron be more closely monitored? If so, this is possible from a social point of view.
Yes. Especially in risk population, brain iron should be more closely monitored. The advantage of QSM is that it can be easily added to the standard MRI test and can be expanded much more than PET. The current challenge is to standardize and use the technology of the scanner and site. Joint efforts are already in progress to move forward. By monitoring brain iron using QSM as an additional improvement, it can be realized at the population level and may be clinically valuable.
