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Background/objectives: Amyloid peptides, whose accumulation in the brain as senile plaques is associated with the onset of Alzheimer's disease, are also found in cerebral vessels and in circulation. In the bloodstream, amyloid peptides promote platelet adhesion, activation, oxidative stress, and thrombosis, contributing to the cardiovascular complications observed in Alzheimer's disease patients. Natural compounds, such as curcumin, are known to modulate platelet activation induced by the hemostatic stimuli thrombin and convulxin.

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Systematic Alzheimer's disease (AD) is a neurodegenerative disease increasingly prevalent in the aging population. AD is characterized by pathological features such as -amyloid (A) plaque accumulation, tau neurofibrillary tangles formation, oxidative stress, an impaired cholinergic system, and neuroinflammation. Many therapeutic drugs have been developed to slow the progression of AD by targeting these pathological mechanisms.

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Targeting Iron Responsive Elements (IREs) of APP mRNA into Novel Therapeutics to Control the Translation of Amyloid-β Precursor Protein in Alzheimer's Disease.

Pharmaceuticals (Basel)

December 2024

Department of Life Science, College of Science and General Studies, Alfaisal University, Riyadh 11533, Saudi Arabia.

The hallmark of Alzheimer's disease (AD) is the buildup of amyloid-β (Aβ), which is produced when the amyloid precursor protein (APP) misfolds and deposits as neurotoxic plaques in the brain. A functional iron responsive element (IRE) RNA stem loop is encoded by the APP 5'-UTR and may be a target for regulating the production of Alzheimer's amyloid precursor protein. Since modifying Aβ protein expression can give anti-amyloid efficacy and protective brain iron balance, targeted regulation of amyloid protein synthesis through modulation of 5'-UTR sequence function is a novel method for the prospective therapy of Alzheimer's disease.

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Florbetaben (FBB) is a radiopharmaceutical approved by the FDA and EMA in 2014 for the positron emission tomography (PET) imaging of brain amyloid deposition in patients with cognitive impairment who are being evaluated for Alzheimer's disease (AD) or other causes of cognitive decline. Initially, the clinical adoption of FBB PET faced significant barriers, including reimbursement challenges and uncertainties regarding its integration into diagnostic clinical practice. This review examines the progress made in overcoming these obstacles and describes the concurrent evolution of the diagnostic landscape.

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Alzheimer's disease (AD) is a progressive neurodegenerative disorder with cognitive dysfunction, memory decline, and behavioral disturbance, and it is pathologically characterized by the accumulation of amyloid plaques and neurofibrillary tangles in the brain. Although various hypotheses have been proposed to explain the pathogenesis of AD, including the amyloid beta hypothesis, oxidative stress hypothesis, and abnormal phosphorylation of tau proteins, the exact pathogenic mechanisms underlying AD remain largely undefined. Furthermore, effective curative treatments are very limited.

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