Abnormal Tau protein
Another important pathological feature is the abnormal aggregation of Tau protein. In healthy neurons, Tau protein helps maintain the stability of the cytoskeleton. But in Alzheimer’s disease, Tau protein abnormally aggregates into tangles, interfering with the normal function of neurons.
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Neuronal damage and death
Aβ deposition and Tau protein abnormalities lead to changes in the internal and external environment of neurons, ultimately causing neuronal damage or even death. This neuronal loss is one of the core causes of cognitive and behavioral symptoms in Alzheimer’s disease.
In addition, inflammatory response, oxidative stress and interneuronal communication disorders are also believed to have an impact on the onset and progression of Alzheimer’s disease.
Overall, the pathogenesis of Alzheimer’s disease is a complex process involving the interaction of multiple molecular, cellular and environmental factors. Scientists are still working hard to understand these mechanisms in order to find preventive strategies for Alzheimer’s disease.
How to intervene
Moderate exercise
As we all know, exercise is positively correlated with health and is one of the important behaviors to improve and maintain our physical health. More and more studies have shown that exercise has many benefits, including helping to prevent cardiovascular and cerebrovascular diseases, metabolic diseases, improving the treatment of various cancers, and having a beneficial effect on a wide range of cognitive functions.
Recently, researchers from the University of Sydney in Australia published a research paper titled “Moderate and vigorous leisure time physical activity in older adults and Alzheimer’s disease-related mortality in the USA: a dose-response, population-based study” in The Lancet Healthy Longevity, a subsidiary of The Lancet.
The study found that engaging in moderate and vigorous physical activity was beneficial in preventing and reducing mortality from Alzheimer’s disease (AD). 20-190 minutes of vigorous exercise per week can significantly reduce Alzheimer’s disease mortality, and 140 minutes of vigorous exercise per week can reduce Alzheimer’s disease mortality by 21%.
In this study, researchers analyzed 91,298 participants aged 68 and older from the National Health Interview Survey cohort, collected their physical activity information through questionnaires, and analyzed the relationship between exercise and Alzheimer’s disease mortality.
The study found no significant dose-response relationship between moderate physical activity and Alzheimer’s disease-related mortality, but a significant L-shaped association between vigorous physical activity and Alzheimer’s disease-related mortality. The study also found that 40 minutes of vigorous physical activity per week could reduce Alzheimer’s disease mortality by 9%, while 140 minutes of vigorous physical activity per week could reduce Alzheimer’s disease mortality by 21% .
According to the results of this study, 12,238 and 37,710 Alzheimer’s-related deaths could be prevented each year in the United States by engaging in 40 minutes and 140 minutes of vigorous physical activity, respectively. In addition, the study also found that 40 minutes and 140 minutes of vigorous physical activity per week could extend the expected survival by 1.6 years and 2.3 years, respectively.
Stem Cell Therapy
At present, the treatment of Alzheimer’s disease is mainly to relieve symptoms, while the root cause of the disease – repairing the irreversible damage of brain neurons – is still a thorny issue. However, a report published in the internationally renowned journal Brain and Behavior some time ago confirmed the potential of mesenchymal stem cells in the treatment of neurocognitive disorders such as Alzheimer’s disease.
Mesenchymal stem cells have strong differentiation and regeneration capabilities and can differentiate into a variety of cell types, including neurons. This property makes them a potential option for treating neurological diseases such as Alzheimer’s disease. Studies have shown that mesenchymal stem cell transplantation can promote the repair of neural function through multiple mechanisms:
Removal of Aβ plaques
Stem cell therapy stimulates enzymes with Aβ-degrading properties, such as enkephalinase, insulin-degrading enzyme, and endothelin-converting enzyme, which helps reduce hippocampal Aβ plaques and thus improves patients’ cognitive sensory functions.
Immunomodulatory effects
Mesenchymal stem cells can accelerate the activation of microglia in the brain, participate in the clearance of Aβ deposits, and thus improve the patient’s cognitive sensory functions.
Anti-inflammatory effects
Stem cell therapy reduces inflammatory factors involved in the chronic inflammatory process, thereby alleviating damage to the brain caused by excessive neuroinflammation.
Inhibition of cell apoptosis
Stem cells can reduce the expression of apoptosis-related factor caspase-3, enhance cell survival signals, and secrete a variety of growth factors, which help reduce Aβ peptide deposition in the brain.
Stem cell differentiation
Stem cells can migrate and differentiate into neuron-like cells, promoting the regeneration and recovery of endogenous neural function.
Secretion of growth factors
The various growth factors secreted by stem cells are believed to have neuroprotective effects on neurodegenerative diseases, helping to improve the microenvironment within the brain, promote nerve regeneration and synaptic regeneration, and combat neurodegeneration.
Combining the above mechanisms of action, stem cell therapy affects neuronal activity, inflammatory response and the removal of Aβ plaques in a variety of ways, bringing hope and the possibility of improving the quality of life to Alzheimer’s patients.
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