Great, great read on how biochemistry effects brain function. Beta-hydroxybutyrate is an alternative fuel source for the brain in times of calorie restriction. This promotes neuroplasticity and neurogenesis without the inflammatory effects of glucose and insulin.
It appears that Levodopa administration in those with Parkinson's disease will deplete methylation (SAMe), and thus increase homocysteine, which is a neurotoxin. Additionally, depletion of methylation is associated with depression, commonly seen in Parkinson's disease
The majority of people with PTHP after TBI remain undiagnosed. The current thought, is that 25% of those with TBI have at least one pituitary hormone deficiency. It does not have to be total pituitary failure. Deficiencies can be isolated.
post-traumatic hypopituitarism is found in 40% of those with TBI. The severity does correlate with the increased likelihood of developing PTHP. Isolated deficiencies have been found in PTHP.
progesterone shown to decrease NF-KappaB and other inflammatory signaling after TBI in rat model. Part of the role of progesterone is as an anti-inflammatory.
allopregnanolone increases human neural stem cells. Not only does allopregnanolone reduce inflammation, it plays a role in neurogenesis and thus recovery.
progesterone shown to provide substantial reduction in volume of infarct in rat stroke model. This is very promising, and with with other studies revealing the same benefit in the human brain, progesterone should become a part of initial treatment in those with acute brain injuries and should be evaluated for those with aging diseases of the brain.
great article on sex hormones and neuroprotection. This article summarizes the research on estrogen, progesterone, and aromatase activity in in vitro and in vivo studies. Additionally, the study reviews the androgenic neuroprotection in men. Who has said that hormones are not needed post menopausal again? Maybe, that is the sign that they need the neuroprotective effect of hormones.
disruption of gut bacteria balance, dysbiosis, proposed to play role in regression autism. This study treated these children with vancomycin. Short interval improvement was found. The take home from this study is the gut-brain connection in children with regression autism
high dose CoQ10 shown to slow disease progression in Parkinson's disease. A similar study had shown the same finding in Huntington's disease. Both are excitotoxic diseases
elevated 2 hour post prandial OGTT associated with all-cause dementia, including Alzheimer's disease. Interestingly, the association was not found with fasting glucose levels.
AGEs are protein modifications that contribute to the formation of the histopathological and biochemical hallmarks of AD: amyloid plaques, neurofibrillary tangles and activated microglia
