36 replies to this topic

[Sleepdealer]

I'm chiming in with Stefan_001 on considering Ginkgo Biloba. It has some positive studies to it, and I don't have Alzheimers disease, but I noticed myself that on the third day of being on it I became, to my surprise, more talkative when around people, and the only side effect that I felt came from it was a weak head ache the first two days for a couple of hours after administration. It might be worth looking into.

 

 

Mitochondrial effects of Ginkgo biloba extract. http://www.ncbi.nlm....pubmed/22784423

 

 

Ginkgo biloba extract ameliorates oxidative phosphorylation performance and rescues abeta-induced failure. http://www.ncbi.nlm....pubmed/20808761

 

 

Ginkgo biloba leaf extract (EGb 761®) and its specific acylated flavonol constituents increase dopamine and acetylcholine levels in the rat medial prefrontal cortex: possible implications for the cognitive enhancing properties of EGb 761®. http://www.ncbi.nlm....pubmed/22784425

 

Edited by Sleepdealer, 26 December 2015 - 02:24 PM.

[noot_in_the_sky]

Here are somethings:

 

Low-Light therapy, You can buy an infrared light on ebay for around 35 dollars.

Source:

http://www.scienceda...21120084729.htm

 

 

UltraSound, you can get on on Ebay it's 1Mhz -I don't know if the frequency is high enough,

Source:

http://news.sciencem...eimer-s-disease

http://pubs.rsna.org...radiol.14142033

 

 

Nilotinib, It's expensive but we are plaining a group buy,

 http://www.longecity...al/#entry755622

http://www.longecity...es/#entry755296

Source:

 http://www.techtimes...-all-in-tau.htm

 

SARM RAD140 

Source:

http://www.ncbi.nlm....les/PMC3959610/

 

Melatonin, but the dose was to high 10mg/kg in mice.

Source:

http://suppversity.b...ts-against.html

 

Estrogen, try getting the body's natural hormone working with SERMs or HRT.

Source:

http://suppversity.b...e-physical.html

 

SERMs, Raloxifene didn't work for women with Alzheimer, it only help to prevent it(120mg/d).

--- Side note, in men SERMs help start the production of hormone specially clomiphene, so SERMs effect on men with Alzheimer may be different.

Source:

http://www.medscape....warticle/853989

 

 

It seems you need to increase blood flow to the brain.

Source:

http://www.nih.gov/n...ding-alzheimers

 

Things to increase blood flow:

Pramiracetam seems to increase the blood flow to the brain the most at 20%(@300mg/kg) alone and 40%(@100mg/kg) w/ lithium, but that much blood is bad.  However, dose amount of pramiracetam where to high as well 100mg/kg is 16.22mg/kg in human & 300mg/kg is 48.65mg/kg in humans.  A good dose is around 2.43mg/kg in a person.

Source:

http://www.ncbi.nlm..../pubmed/8557218

 

Lithium

 

PDE-4 inhibitors, to many to list; one not included is Artichoke Extract, and I believe Viagra & Cialis also helps:

https://en.wikipedia...ibitor#Examples

 

 

Raise Microglia

 

Iron

Source:

https://books.google...croglia&f=false

 

Thyroid Hormone

Source:

http://www.nature.co...l/4000988a.html

[noot_in_the_sky]

I just found this things:

 

Nicotine:

http://www.ncbi.nlm....pubmed/16652343

 

 

Microglial alpha7 nicotinic acetylcholine receptors drive a phospholipase C/IP3 pathway and modulate the cell activation toward a neuroprotective role.

Suzuki T1, Hide I, Matsubara A, Hama C, Harada K, Miyano K, Andrä M, Matsubayashi H, Sakai N, Kohsaka S, Inoue K, Nakata Y.

Abstract

Microglia perform both neuroprotective and neurotoxic functions in the brain, with this depending on their state of activation and their release of mediators. Upon P2X(7) receptor stimulation, for example, microglia release small amounts of TNF, which protect neurons, whereas LPS causes massive TNF release leading to neuroinflammation. Here we report that, in rat primary cultured microglia, nicotine enhances P2X(7) receptor-mediated TNF release, whilst suppressing LPS-induced TNF release but without affecting TNF mRNA expression via activation of alpha7 nicotinic acetylcholine receptors (alpha7 nAChRs). In microglia, nicotine elicited a transient increase in intracellular Ca(2+) levels, which was abolished by specific blockers of alpha7 nAChRs. However, this response was independent of extracellular Ca(2+) and blocked by U73122, an inhibitor of phospholipase C (PLC), and xestospongin C, a blocker of the IP(3) receptor. Repeated experiments showed that currents were not detected in nicotine-stimulated microglia. Moreover, nicotine modulation of LPS-induced TNF release was also blocked by xestospongin C. Upon LPS stimulation, inhibition of TNF release by nicotine was associated with the suppression of JNK and p38 MAP kinase activation, which regulate the post-transcriptional steps of TNF synthesis. In contrast, nicotine did not alter any MAP kinase activation, but enhanced Ca(2+) response in P2X(7) receptor-activated microglia. In conclusion, microglial alpha7 nAChRs might drive a signaling process involving the activation of PLC and Ca(2+) release from intracellular Ca(2+) stores, rather than function as conventional ion channels. This novel alpha7 nAChR signal may be involved in the nicotine modification of microglia activation towards a neuroprotective role by suppressing the inflammatory state and strengthening the protective function.

 

 

 

Cholinergic modulation of microglial activation by alpha 7 nicotinic receptors.

Shytle RD1, Mori T, Townsend K, Vendrame M, Sun N, Zeng J, Ehrhart J, Silver AA, Sanberg PR, Tan J.

Abstract

Almost all degenerative diseases of the CNS are associated with chronic inflammation. A central step in this process is the activation of brain mononuclear phagocyte cells, called microglia. While it is recognized that healthy neurons and astrocytes regulate the magnitude of microglia-mediated innate immune responses and limit excessive CNS inflammation, the endogenous signals governing this process are not fully understood. In the peripheral nervous system, recent studies suggest that an endogenous 'cholinergic anti-inflammatory pathway' regulates systemic inflammatory responses via alpha 7 nicotinic acetylcholinergic receptors (nAChR) found on blood-borne macrophages. These data led us to investigate whether a similar cholinergic pathway exists in the brain that could regulate microglial activation. Here we report for the first time that cultured microglial cells express alpha 7 nAChR subunit as determined by RT-PCR, western blot, immunofluorescent, and immunohistochemistry analyses. Acetylcholine and nicotine pre-treatment inhibit lipopolysaccharide (LPS)-induced TNF-alpha release in murine-derived microglial cells, an effect attenuated by alpha 7 selective nicotinic antagonist, alpha-bungarotoxin. Furthermore, this inhibition appears to be mediated by a reduction in phosphorylation of p44/42 and p38 mitogen-activated protein kinase (MAPK). Though preliminary, our findings suggest the existence of a brain cholinergic pathway that regulates microglial activation through alpha 7 nicotinic receptors. Negative regulation of microglia activation may also represent additional mechanism underlying nicotine's reported neuroprotective properties.

 

 

Menthol:

http://www.sciencedi...014299912001057

 

 

Protective effect of menthol on β-amyloid peptide induced cognitive deficits in mice Abstract

Cognitive impairment is a multidimensional concept that subsumes the attention and concentration, learning and memory, problem-solving ability, visuospatial abilities, mental flexibility, psychomotor efficiency and manual dexterity. The intrinsic mechanisms of the behavioural effects may involve neuronal damage in the brain structure. A lower concentration of glutamate receptor co-agonists in the striatum indicates the general malfunction of the brain glutamatergic system. It is suggested that a selective decrease in hippocampal glutamate concentration may account for deterioration in learning and memory process, considering the important role of this neurotransmitter in the cognitive functions. Nootropic agents like piracetam and anticholinesterase inhibitors are commonly used for improving memory, mood and behaviours. The present study was undertaken to assess the nootropic potential of menthol on learning and memory employing exteroceptive and interoceptive behavioral model in young and aged mice. To delineate the mechanism by which menthol decreases cognitive impairment and protect the brain, various biochemical parameters such as brain glutamate, glycine, glutathione and thiobarbituric acid reactive substances were determined. Menthol produced significant improvement in learning and memory. Menthol exhibited excellent antioxidant effect and maintain glutamate concentration in various region of the mouse brain for management of preliminary symptoms of memory impairment.

 

Galantamine:

 

http://www.ncbi.nlm....les/PMC3001000/

 

Galantamine-induced Amyloid-β Clearance Mediated via Stimulation of Microglial Nicotinic Acetylcholine Receptors

Abstract

Reduction of brain amyloid-β (Aβ) has been proposed as a therapeutic target for Alzheimer disease (AD), and microglial Aβ phagocytosis is noted as an Aβ clearance system in brains. Galantamine is an acetylcholinesterase inhibitor approved for symptomatic treatment of AD. Galantamine also acts as an allosterically potentiating ligand (APL) for nicotinic acetylcholine receptors (nAChRs). APL-binding site is located close to but distinct from that for acetylcholine on nAChRs, and FK1 antibody specifically binds to the APL-binding site without interfering with the acetylcholine-binding site. We found that in human AD brain, microglia accumulated on Aβ deposits and expressed α7 nAChRs including the APL-binding site recognized with FK1 antibody. Treatment of rat microglia with galantamine significantly enhanced microglial Aβ phagocytosis, and acetylcholine competitive antagonists as well as FK1 antibody inhibited the enhancement. Thus, the galantamine-enhanced microglial Aβ phagocytosis required the combined actions of an acetylcholine competitive agonist and the APL for nAChRs. Indeed, depletion of choline, an acetylcholine-competitive α7 nAChR agonist, from the culture medium impeded the enhancement. Similarly, Ca2+ depletion or inhibition of the calmodulin-dependent pathways for the actin reorganization abolished the enhancement. These results suggest that galantamine sensitizes microglial α7 nAChRs to choline and induces Ca2+ influx into microglia. The Ca2+-induced intracellular signaling cascades may then stimulate Aβ phagocytosis through the actin reorganization. We further demonstrated that galantamine treatment facilitated Aβ clearance in brains of rodent AD models. In conclusion, we propose a further advantage of galantamine in clinical AD treatment and microglial nAChRs as a new therapeutic target.

 

Huperzine A:

http://www.ncbi.nlm....les/PMC3077275/

 

 

Huperzine A Activates Wnt/β-Catenin Signaling and Enhances the Nonamyloidogenic Pathway in an Alzheimer Transgenic Mouse Model Abstract

Huperzine A (HupA) is a reversible and selective inhibitor of acetylcholinesterase (AChE), and it has multiple targets when used for Alzheimer's disease (AD) therapy. In this study, we searched for new mechanisms by which HupA could activate Wnt signaling and reduce amyloidosis in AD brain. A nasal gel containing HupA was prepared. No obvious toxicity of intranasal administration of HupA was found in mice. HupA was administered intranasally to β-amyloid (Aβ) precursor protein and presenilin-1 double-transgenic mice for 4 months. We observed an increase in ADAM10 and a decrease in BACE1 and APP695 protein levels and, subsequently, a reduction in Aβ levels and Aβ burden were present in HupA-treated mouse brain, suggesting that HupA enhances the nonamyloidogenic APP cleavage pathway. Importantly, our results further showed that HupA inhibited GSK3α/β activity, and enhanced the β-catenin level in the transgenic mouse brain and in SH-SY5Y cells overexpressing Swedish mutation APP, suggesting that the neuroprotective effect of HupA is not related simply to its AChE inhibition and antioxidation, but also involves other mechanisms, including targeting of the Wnt/β-catenin signaling pathway in AD brain.

 

[Gal220]

Been working with my Mom lately.

 

Tried a few all in one combos like LEF, Jarrow, Mind Lab Pro.

 

Tried Percepta for plaque and tangles.

 

 

Looking at trying BDNF(coffee fruit) and Plasmalogen next

[Turnbuckle]

Been working with my Mom lately.

 

Tried a few all in one combos like LEF, Jarrow, Mind Lab Pro.

 

Tried Percepta for plaque and tangles.

 

 

Looking at trying BDNF(coffee fruit) and Plasmalogen next

 

 

Try this one -- https://www.longecit...-19#entry895287

[Gal220]

Thanks @Turnbuckle

 

I been contemplating how to get her to take your protocol.  We need a Turnbuckle pill...

 

Im not close by and Im not even sure she regularly takes the things I mentioned.

[Daniel Cooper]

I started this thread 6 years ago and thought I'd add somethings I've learned in the interim.

 

My father passed away a bit over 2 years ago.  I was able to do very little to help him.  There was really very little chance of anything I tried to do for him helping. You see, he was diagnosed as having Alzheimer's disease.  But ... he didn't.  In the last few weeks of his life we saw a new attending neurologist and he correctly diagnosed him as having Lewy Body Dementia.   

 

I had been aware that his symptoms did not quite line up with Alzheimer's.  Characteristically prior to the final stages of that disease, most stricken will be able to remember distant memories in the past, but are unable to remember what happened 5 minutes prior. My father never really displayed this pattern. His ability to recall was devastated from the current time all the way back. Also, in his latter stages he started to have hallucinations which is not characteristic of Alzheimer's.  

 

It turns out, that when you've got an elderly patient with dementia, most doctors are not overly interested in determining exactly what kind of dementia it is.  They figure they are very old, and there's little to be done, so they just throw out the diagnosis "Alzheimer's Disease" because everyone's heard of it and most don't ask many questions after receiving it.

 

I regret we didn't receive an accurate diagnosis until the very end (literally in the last two weeks of his life). I don't know if there's anything I could have tried that would have helped, but I definitely would have tried different strategies.  And I think there might have been some things that could have been done to address his hallucinations and anxiety which are not normally features of Alzheimer's.  The fact that these issues were not addressed cause him and my mother undue suffering.

 

I guess my sum up would be, don't necessarily accept a diagnosis of Alzheimer's.  Look at the constellation of symptoms for that disease, and try to determine if they fit. You will be around your loved one far more than any doctor ever will and if things aren't adding up, bring it up with their physician.