I have a genetic predisposition, though at least it doesn't seem to run in my family. I take an interest in things that might help. In addition to GPC and PS:
Selegiline—“The monoamine oxidase-B inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson’s disease and possibly Alzheimer’s disease. The neuroprotective property of L-deprenyl may be unrelated to the inhibition of monoamine oxidase-B. Since nitric oxide (NO) modulates activities including cerebral blood flow and memory, we examined the effect of L-deprenyl on NO. L-Deprenyl induced rapid increases in NO production in brain tissue and cerebral vessels. Vasodilation was produced by endothelial NO- dependent as well as NO-independent mechanisms in cerebral vessels. The drug also protected the vascular endothelium from the toxic effects of amyloid-beta peptide. These novel actions of selegiline may protect neurons from ischemic or oxidative damage and suggest new therapeutic applications for L- deprenyl in vascular and neurodegenerative diseases.”
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PDE5 inhibitor—“Specifically, various rodent studies have reported that PDE5 inhibitors can reverse cognitive impairments and pathology in aged wild-type mice and transgenic Alzheimer’s mouse models through mechanisms including reduced tau hyperphosphorylation (via GSK3β activation), increased BDNF, anti- inflammatory action, increased pCREB signaling, and reduced apoptosis and cell death [2; 3; 4; 5]. Beta- amyloid pathology has been reversed in some [3; 6] but not all [2; 5] studies.
“Whether these effects will occur in humans has yet to be tested. No human studies, observational or randomized, have examined if the use of PDE5 inhibitors can protect against dementia or brain aging.”
Lithium—“One study found that long-term lithium exposure from drinking water may be associated with a lower risk of being diagnosed with dementia. … One epidemiological study in Texas revealed that rates of death from Alzheimer’s were higher in areas with low levels of lithium in the water. In one clinical study, a micro-dose of just 300 mcg of lithium daily was found to significantly decrease cognitive decline in Alzheimer’s patients, compared to a placebo.”
Lithium may slow degenerative processes by inhibiting an age-accelerating enzyme in the brain and other organs.
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Palmitoylethanolamide—(One of two PEAs) “Either preclinical or clinical studies indicate that PEA is potentially useful in a wide range of therapeutic areas, including eczema, pain, and neurodegeneration. … In the present review, we summarized the current preclinical and clinical evidence of PEA as a possible therapeutic agent in Alzheimer's disease. The possible PEA neuroprotective mechanism(s) of action is also described.”
<span><i>N</i>-Palmitoylethanolamide (PEA) is a non-endocannabinoid lipid mediator belonging to the class of the <i>N</i>-acylethanolamine phospolipids and was firstly isolated from soy lecithin, egg yolk, and peanut meal. Either preclinical or clinical studies indicate that PEA is potentially...
pubmed.ncbi.nlm.nih.gov
"Palmitoylethanolamide protects against the amyloid-β25-35-induced learning and memory impairment in mice, an experimental model of Alzheimer disease"
Alzheimer disease (AD) is the most common form of neurodegenerative dementia. Amyloid-β deposition, neurofibrillary tangle formation, and neuro-inflammation are the major pathogenic mechanisms that in concert lead to memory dysfunction and decline ...
www.ncbi.nlm.nih.gov
Vascular dementia and aliamides: A new approach for the future
OA Text is an independent open-access scientific publisher showcases innovative research and ideas aimed at improving health by linking research and practice to the benefit of society.
www.oatext.com
DHEA
Pregnenolone
“Pregnenolone sulfate and DHEA sulfate have also been found to improve cognition in animal studies[111][112][113][114][115][116][117][118]. In an animal model of b amyloid-induced amnesia, DHEA, DHEA sulfate, and pregnenolone sulfate attenuated amnesia in a dose-dependent manner[119]. Interestingly, inhibition of the steroid sulfatase enzyme improved the antiamnesic effect of DHEA sulfate[120][121], indicating that preventing neuroactive steroids from being converted out of their sulfate form may improve cognition.
“Nevertheless, the non-sulfated form of pregnenolone has been shown to improve cognition[122][123] and function[124][125] in schizophrenics. Schizophrenia is characterized by elevations in DHEA and DHEA sulfate and decreases in allopregnanolone, though it is yet unknown how pregnenolone is exerting its effect[126]. It was observed that changes in plasma steroid levels of pregnenolone and allopregnanolone correlated with functional improvements. Interestingly, studies indicate pregnenolone produces biphasic results, where lower dosed (30 mg/day) treatments produced better outcomes than higher dosed treatments (200 mg/day).”
This article introduces the reader to the biosynthesis of neuroactive hormones and reviews what we know about their effects on cognition.
www.leoandlongevity.com
