Disease modification in Parkinson's disease (PD) is an unmet medical need. In the current study, we evaluated trehalose, a safe and well-tolerated disaccharide that has previously demonstrated efficacy in rodent models of neurodegenerative diseases, including PD. In a rat model of PD, based on deliv …

My current research is on Alzheimer's disease (AD) and Parkinson's disease (PD). I believe that these two diseases are related.

We have already reported that glucosamine (GlcN) distinctly abrogates the pigmentation of human epidermal equivalents stimulated by stem cell factor + endothelin-1 (SE). In this study, we characterized the molecular mechanism involved in the anti-melanogenic effects of GlcN using normal human melanocytes (NHMs) in culture. The SE-stimulated gene (12 h) and protein (24 h) expression levels of melanocyte-specific proteins (at the indicated times post-stimulation) were significantly abrogated by pretreatment with GlcN for 72 h. Western blotting analysis of the phosphorylation of intracellular signaling molecules in the MAPK pathway revealed that despite the significantly decreased level of total CREB protein at all times post-stimulation, the SE-stimulated phosphorylation of ERK, CREB and MITF is not attenuated at 15 min post-stimulation in GlcN-treated NHMs. However, the SE-stimulated protein expression level of total MITF at 2 and 6 h post-stimulation was significantly abrogated by 72 h pretreatment with GlcN. Consistently, pretreatment with GlcN for 72 h abrogated the stimulated gene and protein expression levels of MITF at 1 h and 2 h post-stimulation, respectively. Analysis of gene and protein expression levels also demonstrated that pretreatment with GlcN for 72 h significantly reduced the protein levels of CREB and MITF without affecting their gene expression levels prior to the SE stimulation. Silencing with a CREB siRNA distinctly abrogated the SE-stimulated expression of MITF (at 2 h post-stimulation) and melanocyte-specific proteins (at 24 h post-stimulation). Similarly, transfection of MITF siRNA markedly abrogated the SE-stimulated expression of MITF protein and melanocyte-specific proteins at 2 and 24 h post-stimulation, respectively. Finally, the decreased levels of CREB and MITF proteins induced by 72 h pretreatment with GlcN were abrogated by the co-addition of the proteosomal degradation inhibitor MG132. These findings suggest that the anti-melanogenic effect elicited by GlcN is mediated via the decreased expression of MITF which results from the attenuated transcriptional activity of CREB due to proteolytic degradation.

Parkinson’s disease (PD) is the second most common neurodegenerative disease in the elderly, which is clinically characterized by bradykinesia, resting tremor, abnormal posture balance, and hypermyotonia. Currently, the pathogenic mechanism of PD remains unclear. Numerous clinical studies as well as animal and cell experiments have found a certain relationship between the vitamin family and PD. The antioxidant properties of vitamins and their biological functions of regulating gene expression may be beneficial for the treatment of PD. Current clinical evidence indicates that proper supplementation of various vitamins can reduce the incidence of PD in the general population and improve the clinical symptoms of patients with PD; nevertheless, the safety of regular vitamin supplements still needs to be highlighted. Vitamin supplementation may be an effective adjuvant treatment for PD. In this review, we summarized the biological correlations between vitamins and PD as well as the underlying pathophysiological mechanisms. Additionally, we elaborated the therapeutic potentials of vitamins for PD.

We now can convincingly demonstrate that a ketogenic diet is helpful in Parkinson’s, and we now have a better understanding of the underlying mechanisms.

Intermittent Fasting has been shown to reduce whole body inflammation. Discover how intermittent fasting improves brain function.

The enzyme serrapeptase is used to relieve pain and inflammation; its effects on heart health are also being researched. Learn more here.

Neurons affected in Alzheimer’s disease (AD) experience mitochondrial dysfunction and a bioenergetic deficit that occurs early and promotes the disease-defining amyloid β-peptide (Aβ) and Tau pathologies. Emerging findings suggest ...

Older adults with low intake of foods and drinks containing flavonoids, such as berries, apples, and tea, were more likely to develop Alzheimer's disease and related dementias over 20 years, compared with people who consumed more of those items, according to a new study.

A supplement that stops the breakdown of the ACh neurotransmitter in the brain is a useful technique to trigger lucid dreams

Dr. Dale Bredesen has shown, using lifestyle changes like a ketogenic diet, that Alzheimer's Disease and dementia can be prevented and reversed.

Alzheimer's disease (AD) is a leading killer of Americans, imparts a significant toll on the quality of life of the patient and primary caregiver, and results in inordinate costs in an already overburdened medical system. Prior studies on cholinesterase inhibitors among AD patients have shown minima …

Intermittent Fasting has been shown to reduce whole body inflammation. Discover how intermittent fasting improves brain function.

Transgenic mice with increased amyloid-β (Aβ) production show several aspects of Alzheimer’s disease, including Aβ deposition and memory impairment. By repeatedly treating these Aβ-forming mice with scanning ultrasound, Leinenga and Götz now demonstrate that Aβ is removed and memory is restored as revealed by improvement in three memory tasks. These improvements were achieved without the use of any therapeutic agent, and the scanning ultrasound treatment did not induce any apparent damage to the mouse brain. The authors then showed that scanning ultrasound activated resident microglial cells that took up Aβ into their lysosomes. These findings suggest that repeated scanning ultrasound may be a noninvasive method with potential for treating Alzheimer’s disease. Amyloid-β (Aβ) peptide has been implicated in the pathogenesis of Alzheimer’s disease (AD). We present a nonpharmacological approach for removing Aβ and restoring memory function in a mouse model of AD in which Aβ is deposited in the brain. We used repeated scanning ultrasound (SUS) treatments of the mouse brain to remove Aβ, without the need for any additional therapeutic agent such as anti-Aβ antibody. Spinning disk confocal microscopy and high-resolution three-dimensional reconstruction revealed extensive internalization of Aβ into the lysosomes of activated microglia in mouse brains subjected to SUS, with no concomitant increase observed in the number of microglia. Plaque burden was reduced in SUS-treated AD mice compared to sham-treated animals, and cleared plaques were observed in 75% of SUS-treated mice. Treated AD mice also displayed improved performance on three memory tasks: the Y-maze, the novel object recognition test, and the active place avoidance task. Our findings suggest that repeated SUS is useful for removing Aβ in the mouse brain without causing overt damage, and should be explored further as a noninvasive method with therapeutic potential in AD.

Dr. David Perlmutter, author of Grain Brain, interview Dr. Dale Bredesen, the author of The End of Alzheimer's and a medical pioneer.

The End of Alzheimer's Program: The First Protocol to Enhance Cognition and Reverse Decline at Any Age [Bredesen, Dale, Perlmutter, David] on Amazon.com. *FREE* shipping on qualifying offers. The End of Alzheimer's Program: The First Protocol to Enhance Cognition and Reverse Decline at Any Age

Today’s short video clip with Dr. Daniel Stein, dives deep into how to TREAT this horrific disease. You’ll discover the exact cannabinoids, terpenes and dosage protocol Dr. Stein recommends... *** This limited clip is a preview from our Healing Brain Masterclass. Get full access to our entire 3 masterclass library, complete season 1 docuseries, and over 37 bonuses on a portable 100+ GB flash drive... Go here for all the details 👉 http://bit.ly/2rl3F33

Abnormal accumulation of amyloid proteins is linked to neuronal degeneration in Alzheimer's disease brains, driving cognitive decline. Disruption of autophagy pathway contributes to the development o...

Although the potential contribution of the human gastrointestinal (GI) tract microbiome to human health, aging, and disease is becoming increasingly acknowledged, the molecular mechanics and signaling pathways of just how this is accomplished is not well-understood. Major bacterial species of the GI tract, such as the abundant Gram-negative bacilli Bacteroides fragilis (B. fragilis) and Escherichia coli (E. coli), secrete a remarkably complex array of pro-inflammatory neurotoxins which, when released from the confines of the healthy GI tract, are pathogenic and highly detrimental to the homeostatic function of neurons in the central nervous system (CNS). For the first time here we report the presence of bacterial lipopolysaccharide (LPS) in brain lysates from the hippocampus and superior temporal lobe neocortex of Alzheimer's disease (AD) brains. Mean LPS levels varied from two-fold increases in the neocortex to three-fold increases in the hippocampus, AD over age-matched controls, however some samples from advanced AD hippocampal cases exhibited up to a 26-fold increase in LPS over age-matched controls. This “Perspectives” paper will further highlight some very recent research on GI tract microbiome signaling to the human CNS, and will update current findings that implicate GI tract microbiome-derived LPS as an important internal contributor to inflammatory degeneration in the CNS.

Alzheimer's disease is an irreversible and progressive brain disorder featured by the accumulation of Amyloid-β (Aβ) peptide, which forms insoluble assemblies that builds up into plaques resulting in cognitive decline and memory loss. The formation of fibrillar amyloid deposits is accompanied by con …

A new study in the journal Neurology explores the scientific fact behind the relationship between vitamin D and dementia and Alzheimer's

In California, people with Alzheimer's will be given transfusions of young blood to see if improves their cognition – there's good reason to hope it might

Alzheimer's disease is expanding unchecked throughout the modern world, despite billions spent annually on pharmaceutical interventions. Could the calcification of the brain play a role?