Alzheimer’s Prevention Trials—The Future Looks Promising

Alzheimer’s Prevention Trials—The Future Looks Promising

While there is active research for more effective disease-modifying drugs* the lack of any significant breakthroughs in the treatment of the Alzheimer’s disease has propelled a paradigm shift away from focusing solely on a drug solution, to an inclusive prevention model that emphasizes risk reduction and prevention, which promises to attenuate the portentous global burden incurred by the disease.

Current prevalence estimates (2016) 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.
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MEMBER ACCESS: Mercury Depletes Glutathione Peroxidase-Toxic Mechanisms In Alzheimer’s Disease Risk

MEMBER ACCESS: Mercury Depletes Glutathione Peroxidase-Toxic Mechanisms In Alzheimer’s Disease Risk

The research demonstrating the deleterious and toxic effects of mercury on brain function and struct...

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MEMBER ACCESS: Oxidative Stress and the Thromboxane Receptor—A Central Pivot in the Production of Neurofibrillary Tangles

MEMBER ACCESS: Oxidative Stress and the Thromboxane Receptor—A Central Pivot in the Production of Neurofibrillary Tangles

New research published Oct. 13 (2014) by the journal Neurobiology of Aging revealed that the free ra...

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MEMBER  ACCESS: TREM2 genetic variants in Alzheimer’s disease

MEMBER ACCESS: TREM2 genetic variants in Alzheimer’s disease

Two recently published studies (2013) on a rare variant of the TREM2 gene (triggering receptor expre...

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Inflammation and Alzheimer’s Disease—Cause, or Effect?

Inflammation and Alzheimer’s Disease—Cause, or Effect?

The role of chronic inflammation in degenerative diseases associated with aging is considered to be a primary vector for the progression of neurodegenerative disorders and a powerful factor that underlies their etiology.

One needs only to look at the leading causes of mortality—heart disease and stroke, and the research models of inflammation that clearly link the pathogenesis of these disease processes in aging individuals to understand that inflammation and chronic degenerative disease are inseparable.

Since inflammation is central to aging-associated disease processes, it has been heavily investigated in models of neurodegeneration. In Alzheimer’s disease,  several studies have sought to clarify whether inflammation is a causative stimulus, or a concomitant feature of the disease process. (more…)

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