FAQs: Preserving Cognitive Function/Preventing Neurodegeneration

  1. Neurosupportive Potential of Creatine Orotate

    This essay proposes that the supplement creatine orotate may work in multiple complementary ways to aid cognitive function, while protecting the brain from stroke, trauma, and neurodegenerative disorders, and also supporting efficient brain healing. It should do this by boosting brain levels of key metabolic constituents – pyrimidines, carnosine, and creatine – that support efficient function and provide protection.

  2. Adjuvant Strategies for Managing ALS

    Amyotrophic lateral sclerosis (ALS) is a devastating and mysterious neurological disease in which the central nervous system gradually loses control of the body’s musculature, owing to progressive death of the motor neurons controlling muscles. Although no cure for this disorder is on the horizon, this essay proposes that measures such as high caffeine intake, supplementation with inosine and spirulina, and an innovative and practical anti-inflammatory treatment strategy – known as “Tolovax” – may have potential for slowing the progression of ALS.

  3. Practical Strategies for Preserving Good Cognitive Function into Old Age

    As people age, there is a tendency for cognitive ability to decline at least modestly, and, in many people, neurodegenerative disorders and/or strokes can bring on dementia. This article suggests a wide number of lifestyle strategies – involving dietary choices, exercise, nutraceuticals, and drugs – that have potential, particularly if implemented in mid-life, to minimize risk for age-related cognitive decline and dementia. A concluding section summarizes these measures, and classifies them as first-line (feasible for primary prevention in healthy people), second-line (to be considered when the onset of cognitive decline is noted), and third-line (for consideration if cognitive decline continues to progress.)

    Updated posting, September 2013

  4. The Neuroinflammation and Loss of Hippocampal GABAergic Interneurons That Mediate Age-Related Decline in Cognitive Function May be Interdependent

    This article discusses the neurological mechanisms which are suspected to bring on the cognitive decline associated with healthy aging – in particular, the mild brain inflammation associated with the chronic activation of microglial cells (neuroinflammation), and the die off of certain neurons that produce the neurotransmitter GABA. Practical strategies for mitigating these effects, and hence slowing or prevening age-related cognitive decline, are suggested.

  5. A Role for Activated Microglia and Peroxynitrite in Lewy Body Disease – Implications for Prevention and Control

    Parkinson’s disease and Lewy body dementia – a little-publicized disorder thought to be responsible for about 20% of clinical dementia – may be two aspects of the same underlying problem, Lewy body disease, characterized by aggregation of the protein alpha-synuclein into intraneuronal inclusions known as Lewy bodies. This article proposes that inflammatory activation of brain cells known as microglia, and the highly toxic pro-oxidant compound peroxynitrite, produced by these activated microglia, may collaborate to induce and sustain Lewy body disease. Various antioxidant and anti-inflammatory nutraceuticals, drugs and lifestyle measures are discussed which have potential for scavenging peroxynitrite and dampening microglial inflammation.

  6. Taurine, A Natural LXRalpha, May Promote Amyloid Beta Clearance in the Brain

    There is very recent evidence that the nutrient taurine can activate an intracellular receptor known as LXRalpha. Certain drugs capable of activating this receptor – not yet available clinically – are beneficial in rodent models of Alzheimer’s disease, largely because they promote degradation of toxic amyloid beta protein complexes by brain microglial cells. It is proposed that high-dose supplementation with non-toxic taurine may have similar protective potential.

  7. Tributyrin May Have Practical Potential for Improving Cognition in Early Alzheimer’s Disease Via Inhibition of HDAC2

    Recent research at MIT has determined that, in rodent models of Alzheimer’s dementia, the negative impact of amyloid beta exposure on neuronal function and new memory formation results largely from increased neuronal expression of an enzyme known as HDAC2 (histone deacetylase 2). A class of drugs and metabolites known as class I histone deacetylase inhibitors have the potential to inhibit the activity of HDAC6 and thereby favorably impact memory. This article reviews those drugs, and suggests that, in light of the high cost of certain other options, an approved food additive known as tributyrin may have the most practical potential in this regard.

  8. Memo: Arian Foster’s Whole-Food Vegan Diet May Protect Him from Trauma-Triggered Neurodegenerative Disorders

    Professional football players, and other people whose professions may subject them to repeated moderate brain trauma, are now known to be at increased risk for neurogenerative disorders – particularly Alzheimer’s and ALS – during their retirement years. There is evidence that chronic mild brain inflammation, triggered by repeated injuries, may be the chief driver of this risk. This article cites some practical measures which may help to prevent or ameliorate this chronic inflammation, and in particular focuses of the protective potential of vegan or Mediterranean diets low in saturated fats, which may help to control production of a group of pro-inflammatory compounds known as ceramides.

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