Alzheimer’s Prevention Trials—The Future Looks Promising

Alzheimer’s Prevention Trials—The Future Looks Promising

Current prevalence estimates for late-onset Alzheimer’s disease LOAD in the United States (U.S.) is approximately 5.1 million.(1) By 2050 the projected prevalence of LOAD is expected to escalate to 13.8 million and a staggering 106.8 million worldwide.(2,3) Pharmacological treatments for LOAD such as cholinesterase inhibitors and NMDA receptor antagonists may slow its progression or attenuate specific molecular pathomechanisms associated with the disease process, but are not long term solutions or curative. While there is active research for more effective disease-modifying drugs* the lack of any significant breakthroughs in the treatment of the disease has propelled a paradigm shift away from focusing solely on a pharmaceutical solution to an inclusive prevention model that emphasizes risk reduction and ultimately the portentous global burden incurred by the disease.

Several clinical trials have recently explored the potential role of prevention-based interventions for decreasing the risk of late-onset Alzheimer’s disease (LOAD) and vascular dementia. The outcomes are encouraging. Multi-dimensional interventional strategies (implementing multiple treatment and prevention modalities simultaneously) versus mono-therapy (employing only with a single treatment modality e.g. drugs) has yielded promising results in reducing the eventual onset of dementia for aging individuals considered to be at higher risk. These trials highlight the potential effectiveness of preventive approaches for individuals deemed to have a higher risk for vascular dementia and LOAD and for the management of Mild Cognitive Impairment (MCI).**

Oxidative Stress and the Thromboxane Receptor–A Central Pivot in the Production of Neurofibrillary Tangles and Amyloid-beta

Oxidative Stress and the Thromboxane Receptor–A Central Pivot in the Production of Neurofibrillary Tangles and Amyloid-beta

By Ralph Sanchez, MTCM, CNS, D.Hom.

New research published Oct. 13 by the journal Neurobiology of Aging revealed that the free radicals produced during oxidative stress bind to a protein receptor in the brain designated as “the Thromboxane Receptor A2 (TP)”. The study, “Modulation of AD Neuropathology and Memory Impairments by the Isoprostane F2α Is Mediated by the Thromboxane Receptor” demonstrated that oxygen free radicals actually bind to TP, and transmit signals to neuronal cells to increase the production of amyloid beta, and Neurofibrillary Tangles (abnormal phosphorylated microtubule-associated protein tau), the two major pathological lesions associated with Alzheimer’s disease. See illustration just below.

Plaques and Tangles in the Alzheimer’s Brain-Which One Is Most To Blame For Alzheimer’s Disease?

Plaques and Tangles in the Alzheimer’s Brain-Which One Is Most To Blame For Alzheimer’s Disease?

The two hallmark lesions that are associated with the damage that occurs in Alzheimer’s disease (AD) are neurofibrillary tangles and amyloid plaques (see pic 1). Processes involving inflammation, oxidative stress, * mitochondrial dysfunction, ** brain cholesterol dynamics (1) and others are tied into the formation of plaques and tangles. However, there has been a long-standing debate in the research community as to whether one lesion or the other is primarily responsible for the AD process.

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