![]() Familial AD is an early-onset autosomal dominant genetic disease. APP mutations have been confirmed to be associated with hereditary familial AD. The accumulation of Aβ into plaques and smaller oligomers is one of the pathological features of AD. The first is Aβ, which is a pathological cleavage product of amyloid precursor protein (APP). Studies have shown that two typical misfolded proteins accumulate in the brain of patients with AD. This review focuses on the mechanisms of AD pathogenesis and discusses clinical and preclinical findings on the role of stem cells in the treatment of AD. They are considered to be the most suitable choice to provide uniform and unique cells required for cell replacement therapy. Current breakthroughs in preclinical research and clinical trials of stem cells have ignited hope for the treatment of refractory neurodegenerative diseases such as AD. At the same time, it is also necessary to provide a better environment for the remaining cells. Therefore, new and effective treatments, such as removing toxic deposits and replacing lost neurons, need to be developed to improve the pathological state of the disease, stimulate neural precursors, prevent nerve death, enhance structural neural plasticity, and so forth. However, it is unclear how valuable such a palliative drug-based approach can be. In fact, currently available treatments include three types of cholinesterase inhibitors, one N-methyl-daspartate receptor antagonist, and one combined drug therapy (memantine plus donepezil) are currently approved for clinical use. Reducing Aβ levels has been the dominant treatment strategy in development to halt, retard, or even reverse the progression of AD pathology. Accordingly, the results of CSF biomarkers for AD may provide explanatory evidence for neurocognitive symptoms and predict the type of evolution, especially when there are no other obvious causes of cognitive impairment. These criteria highlight that the gold standard for the etiological diagnosis remains the neuropathological assessment. ![]() ![]() Although cerebrospinal fluid (CSF) and positron emission tomography (PET) biomarkers combined with some relatively new clinical standards can help diagnose alive patients, the certainty of diagnosis was achieved only by post-mortem autopsy. ![]() Despite advances in understanding the etiology of AD, treating the disease by retaining acetylcholine and reducing glutamate is limited to symptom management. With a new case occurring every 3 s worldwide, AD has rapidly become an epidemic, with the number of cases predicted to be 152 million by 2050.ĪD has several neuropathological hallmarks, including the deposition of β-amyloid (Aβ) peptides in the extracellular matrix between neurons (known as amyloid plaques), the intracellular formation of neurofibrillary tangles arising from the accumulation of hyperphosphorylated tau protein in neurons, neuronal loss, neuroinflammation, and oxidative stress. The 2018 World Alzheimer's Disease Report shows that 50 million people worldwide have dementia. Alzheimer's disease (AD) is the most common cause of dementia, accounting for 50%-70% of dementia cases worldwide. This paper reviews the pathophysiology of AD and the application prospects of related stem cells based on cell type.ĭementia is a neurodegenerative, debilitating, and fatal disease characterized by progressive cognitive impairment, behavioral disorders, and loss of function in daily life. However, many steps still need to be taken before stem cell therapy becomes a clinically feasible treatment for human AD and related diseases. Cell replacement therapies, such as human embryonic stem cells or induced pluripotent stem cell–derived neural cells, have the potential to treat patients with AD, and human clinical trials are ongoing in this regard. Recent preclinical studies on stem cell therapy for AD have proved to be promising. Stem cell treatment has been successful in AD animal models. Stem cells have improved characteristics of self-renewal, proliferation, differentiation, and recombination with the advent of stem cell technology and the transformation of these cells into different types of central nervous system neurons and glial cells. Also, currently available drug candidates intervene too late. To date, almost all advanced clinical trials on specific AD-related pathways have failed mostly due to a large number of neurons lost in the brain of patients with AD. It is caused by synaptic failure and excessive accumulation of misfolded proteins. Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by memory loss and cognitive impairment. ![]()
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