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  1. #1
    Senior Member akp2004's Avatar
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    This community means much to me.

    I just talked with my mom.

    My dad''s 86 -- hiz mom died at 93 so not expecting early death. So, short of accepting we put him in a carefacility, what is the most up to date research and speculative resarch that focused or can keep early Alzheimer's stable for as long as possible.



    Pharmaceutical

    Nootropic/Alternative



    This is a huge pain in our family.



    I know this info is spread among the board in fragments. i need a collective summary

    documented medical studies, and summarize current suggested treamtments, that i can presenf to my dad and his treatment team..



    I will pay for time invested in those who collect studies - my dad's a former research professor and is not going to take a recommendation like "galantamine has been shown to be helpful." I pay well for proper research.



    I will also donate money if that's not your driving force.



    Please - I need help - Mom is at breaking point, and anything is appreciated; I am working to the bone.

    Connecting to my dad intellectually was our main way of bonding - this is very painful



    I believe he was on Aricept (no change),now on Exelon (sp?)



    Please trust too, if I pay you, I will sign an NDA that has terms of non medical advice, or rewrite so it comes from me.. This is not an entrapment bullshit... Just reaching out for help, that crosses a bit into the disease treatment questions





    --please pm me or post in the thread.







    EDIT: Saturday morning --- I appreciate Klee and Eclypz's post. I think the money thing was motivated by sheer shock, and wanting a fast solution - I also know time is tight for alot of people. But thank you for your expression around community ethos around helping for the sake of helping.

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    Senior Member eclypz's Avatar
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    Quote Originally Posted by akp2004' post='373164' date='Nov 22 2006, 07:16 PM

    i need a collective summary

    documented medical studies, and summarize current suggested treamtments, that i can presenf to my dad and his treatment team..


    Dude, you know what we know mostly. Contact someone privately if you need to, but I'm willing to bet most of us would be more than happy to share what we know for free - knowing it's going to help someone finish their life gracefully.



    Here's what I think any of us know; Alzeihmer's has not yet been cured. I know it sounds basic, but let's start off the bat knowing the most we can do is to give your father the best damn life he can have at this point.



    I know ATB has been spending alot of time looking at the pathology of alzeihmer's in terms of how it comes about, alot of stuff about inflammation and the signals it sets off.



    ========================================



    What do we know about treating it once it's present?



    -------------------------------------------------------------------



    Here's what I know, and I have no studies to back it up so you can tell your dad not to pay attention to any of this unless it just makes sense.



    Diet: No matter what your father decides to do in terms of pharmaceutical treatment, I think he should understand the role that excess blood sugar plays in health overall. There are studies after studies that show a well balanced diet is crucial. Keeping insulin under control means keeping alot of inflammatory pathways under control. Those pathways can exacerbate any underlying condition.



    I actually think your galantamine suggestion is a good one. Do I have studies to back it up? no. There are plenty out there though, just hit up pubmed. There are also studies showing ace inhibitors in general are good for this situation. Somethng affecting dopamine might be good as well. The problem is, alzeihmers is an engimatic disease that calls for a multitude of pharm's and those only treat the symptoms in my opinion.



    Perhaps this post will serve as nothing but a calling to those who can help, and I'm sure any of us would do it for free knowing we could help.

  3. #3
    Senior Member spike77's Avatar
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    The following link has lot of info - I personally try to update it with everything new and interesting that I find and ATB (who started the thread) is your man!



    http://www.avantlabs.com/forum/index...howtopic=23153
    To cut the Gordian knot.

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    Senior Member noos's Avatar
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    I don´t think this will "treat" Alzheimer´s, but if you want to convince him (I doubt you can if he is not already interested) that there is some scientific bssis for cognitive supplementation you could mention that there are research scientists involved in the study/development of drugs/compounds:



    Nobel prize Eric Kandel

    http://www.businessweek.com/magazine/conte...47001_mz001.htm





    Richard Wurtman from MIT

    http://web.mit.edu/bcs/people/wurtman.shtml

    Some research on Alzheimer´s and on precursors, values CDP-choline (not specifically for AD, an intersting and "natural" product).





    Bruce Ames, University of California, Berkeley

    Researched (and sells) ALC+ALA

    http://www.juvenon.com/



    At www.lef.org there are protocols for almost everything.

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    Senior Member Benson's Avatar
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    Just a couple of directionals that might lead you someplace useful.



    Huperzine A appears to have protective effects against AD that go well beyond its AChE inhibitory effects. To me, this particular substance looks very promising as a treatment for slowing the progression of the disease.



    A large Canadian study found that the incidence of AD is inversely related to caffeine exposure. Whether this means that caffeine itself may halt the progression of the disease is unknown but it may provide some clues about its etiology that can be useful.



    Lastly, there has been a small but significant body of work since the mid 90's that indicate that nicotine use may improve the prognosis for Alzheimer's patients. Smokers respond better to treatment than non-smokers and a couple of small studies of nicotine patches with both AD patients and those with age-linked memory decline showed encouraging improvements...
    Remember, believe none of what you hear and half of what you see...





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    Well there's quite a few avenues to research.



    I could start by listing a few of them. Not all have direct evidence they work, some is via animal models, and some is through other diseases thought to have common mechanisms with AD, and some is via epidemiological research.



    The obvious stuff, whistle stop tour, remember that this field is being informed by more recent research, so reserach is quite shallow on many potential therapies;



    Berries, blueberries and blackberries for example, have compounds that block an important mechanism in neurodegeneration - that of peroxynitrite and hydrogen peroxide.



    Frozen blueberries and you could look out for other fruit like Acai. These fruits seem to help protect the brain, and are known to work centrally.



    2 portions a day should cover that.



    Curcumin has been linked at stopping the inflammatory process and protecting in epidemiological research on the rates of AD.



    Curcumin may block inflammatory signaling and it may actually help lower amyloid.



    Curry eating has been strongly linked to lower incidence of AD. Several compounds may be responsible as well, i.e. cumin, which seems to be a potent anti-inflammatory.



    Some researchers have suggested gamma tocopherol. A good supplement therefore might by Jarrows antioxidant formula, since it contains curcumin, grape seed extract and also gamma tocopherol. (I am in no way involved in that company).



    However, grape seed extract and Carnosine may be important neuroprotectants. Carnosine has some promising research in a different but also inflammation connected condition, autism. It appears to raise brain metabolism and improve sociability. Substances in grape seed extract also has some research showing benefits in other conditions, potentially relevant.



    Ibuprofen - I've got a thread on it, http://www.mindandmuscle.net/forum/i...howtopic=23166



    DHEA - this molecule suppresses aspects of neuro-inflammation. Levels decline with age.



    Magnesium, Omega 3 fatty acids, both important. Omega 3's with a higher ratio of EPA would be indicated. Mackerel, small fillets from the Atlantic are low in pollutants, cheap, and lack the strong taste of other O3 rich fish. The EPA and DHA are needed. EPA may function through common anti-inflammatory mechanisms as above.



    Now, the research indicates that AD is a condition characterised by sub-requirement metabolism for neural activities. That is, via a metabolic impairment, via mitochondrial dysfunction, proteome dysfunction, transport dysfunction, lack of oxygen, and insulin/signaling problems, neurons rapidly suffer 'proteome' damage and part of that appears in the form of amyloid and tau and the most toxic abnormal protein accumulation is that inside the cell. Then, the metabolic abnormalities hit nerve cells again as they cannot regulate activity properly and are more likely to die. Glia are likely to be effected the same way at the same time, this they too may be mal-regulated. After the damage to the neurons, inflammation by glia ensures increased damage.



    One of the central aspects of this appears to be impaired metabolism. Brain cell activity also blocks inflammatory actions by glia and dysregulation and hypo-activity of neurons also will logically excacerbate this cascade.



    For that reason, it might be worth looking at restricting excess calories and carbohydrate/sugar.



    Lower calorie intake also protects against these proteins.



    DHEA may be beneficial in another way - that is, it might improve mood, which if an issue, could be problematic since stress also worsens the condition, and DHEA may be of benefit there. Good sleep is important since lack of it and lack of sleep rhythms will worsen the situation all round. Should be taken in the morning.



    Going back to the metabolic aspect of the condition, the use of chromium may be beneficial, since it appears also to act centrally at raising mood and reducing carbohydrate cravings and is known to improve insulin sensitivity. Also, selenium.



    Niacin and Niacinamide appear to be highly neuro-protective, and beneficial in AD. Folic acid may offer benefits also. Niacinamide has been shown also to be very protective in animal models of MS.



    Boron may be beneficial along with magnesium to prevent neural dysfunctions that may result in cell death.



    Connected to metabolism, R Lipoic Acid, and Acetyl L Carnitine are well known from exciting research showing they could reverse age related declines. Phosphatidyl Serine has also been implicated the same way, though that may be largely replicated by DHA alone.



    Now, the exciting bit. This is just an article but it covers it;



    PPAR Delta.




    http://www.eurekalert.org/pub_releas...-irs092106.php



    Insulin receptor stops progression of Alzheimer's disease



    Patients could be treated in early phases of disease



    Providence, RI – Stimulation of a receptor in the brain that controls insulin responses has been shown to halt or diminish the neurodegeneration of Alzheimer's disease, providing evidence that the disease can be treated in its early stages, according to a study by researchers at Rhode Island Hospital and Brown Medical School.



    Researchers have found that peroxisome-proliferator activated receptor (PPAR) agonists prevent several components of neurodegeneration and preserve learning and memory in rats with induced Alzheimer's disease (AD). They found that an agonist for PPAR delta, a receptor that is abundant in the brain, had the most overall benefit.



    "This raises the possibility that you can treat patients with mild cognitive impairment who have possible or probable Alzheimer's disease. This is really amazing because right now, there's just no treatment that works," says lead author Suzanne M. de la Monte, MD, MPH, a neuropathologist at Rhode Island Hospital and a professor of pathology and clinical neuroscience at Brown Medical School in Providence, RI.



    The study appears in the September issue (Volume 10, Issue 1) of the Journal of Alzheimer's Disease (www.j-alz.com).



    In previous studies, the researchers demonstrated that Alzheimer's is a brain-specific neuroendocrine disorder, or a Type 3 diabetes, distinct from other types of diabetes. They showed that insulin and IGF-I receptors are produced separately in the brain, and begin to disappear early in Alzheimer's and continue to decline as the disease progresses. As insulin signaling breaks down, it leads to increased oxidative stress, impaired metabolism and cell death – all causing neurodegeneration.



    Scientists were also previously able to replicate Alzheimer's in rats with Streptozotocin (STZ), a compound that is known to destroy insulin producing cells in the pancreas and cause diabetes. When injected into the brains of rats, the compound mimicked the neurodegeneration of Alzheimer's disease – plaque deposits, neurofibrillary tangles, diminished brain size, impaired cognitive function, cell loss and overall brain deterioration.



    Having created an animal model for Alzheimer's, researchers in this study induced Alzheimer's with STZ and then administered treatment with three classes of PPAR agonists – alpha, gamma and delta. All are found in various tissues and organs in the body, including the brain, and PPAR gamma is already FDA approved as a treatment for Type 2 diabetes, or adult-onset diabetes. The two other classes of PPAR agonists have not yet been approved for clinical use.



    Following treatment, many of the abnormalities associated with Alzheimer's were reduced or nearly disappeared. The agonists affected different regions of the brain, with PPAR delta producing the most striking effect in preserving the hypothalamus and temporal lobes, areas of the brain responsible for memory, learning, and behavior. In these brain regions, PPAR alpha and PPAR gamma were effective in reducing amyloid gene expression. PPAR delta had the most benefit for reducing oxidative stress and improving learning and memory.



    "That was the most spectacular," de la Monte says, "because everybody wants something for cognitive impairment, and that was the most improved with the PPAR delta agonist."



    Researchers were not able to stop the deterioration of insulin and its receptors. However, by administering PPAR, they were able to bypass the defects in insulin signaling and preserve the cells that need insulin to thrive. PPAR molecules go directly to the nucleus of cells and tell DNA to turn on or off genes that are normally regulated by insulin, thus preventing them from dying and allowing them to communicate with each other. The major effects of the PPAR treatments were to increase brain size, preserve insulin and IGF-II receptor bearing neurons, and preserve learning and memory.



    "The trigger for dementia is the loss of insulin and IGF producing cells. The cells that need those growth factors subsequently die. This study shows you can block the second phase, which is responsible for dementia. This is great news for patients since you treat early stages of disease," de la Monte says.



    Another promising result for Alzheimer's patients is that these drugs could be given in the form of a pill, de la Monte says. In the study, the drugs were injected to control the amounts administered.



    "One of the most exciting findings was that peripheral (intraperitoneal) injection of the PPAR agonists either partially or completely rescued the brains from neurodegeneration," the authors write.



    Alzheimer's appears to be caused by parallel abnormalities – impaired insulin signaling and oxidative stress, which is regulated by the genes NOS and NOX. The PPAR agonists treatments target both problems. They preserve the cells regulated by insulin and IGF, and they decrease oxidative stress, resulting in fewer lesions in the brain.



    "If the diagnosis is suspected or patients are in the early phases of AD, there's a good possibility they could get treatment that will help them. It's possible that in the moderate phase, treatment will also help, but more work needs to be done to show that," de la Monte says.



    Treatment is not likely to work in the late stages of the disease, she says, because the cells have already died.


    Sounds good?



    PPAR delta also seems to stimulate cells to differentiate into oligodentocytes, which is another very nice action.



    So what increases it?



    Step forward Vitamin D;




    The human peroxisome proliferator-activated receptor delta gene is a primary target of 1alpha,25-dihydroxyvitamin D3 and its nuclear receptor.



    Drs. Paul Sternberg and Franco Recchia evaluate possible changes in ophthalmic practice with anti-VEGF agents; Dr. Paul Latkany presents an unusual case; Dr. Robert Bernardino reviews the literature.



    J Mol Biol. 2005; 349(2):248-60 (ISSN: 0022-2836)

    Dunlop TW; Väisänen S; Frank C; Molnár F; Sinkkonen L; Carlberg C

    Department of Biochemistry, University of Kuopio, FIN-70211 Kuopio, Finland.



    Peroxisome proliferator-activated receptor (PPAR) delta is the most widely expressed member of the PPAR family of nuclear receptor fatty acid sensors. Real-time PCR analysis of breast and prostate cancer cell lines demonstrated that PPARdelta expression was increased 1.5 to 3.2-fold after three hours stimulation with the natural vitamin D receptor (VDR) agonist, 1alpha,25-dihydroxyvitamin D3 (1alpha,25(OH)2D3). In silico analysis of the 20 kb of the human PPARdelta promoter revealed a DR3-type 1alpha,25(OH)2D3 response element approximately 350 bp upstream of the transcription start site, which was able to bind VDR-retinoid X receptor (RXR) heterodimers and mediate a 1alpha,25(OH)2D3-dependent upregulation of reporter gene activity. Chromatin immuno-precipitation assays demonstrated that a number of proteins representative for 1alpha,25(OH)2D3-mediated gene activation, such as VDR, RXR and RNA polymerase II, displayed a 1alpha,25(OH)2D3-dependent association with a region of the proximal PPARdelta promoter that contained the putative DR3-type VDRE. This was also true for other proteins that are involved in or are the subject of chromatin modification, such as the histone acetyltransferase CBP and histone 4, which displayed ligand-dependent association and acetylation, respectively. Finally, real-time PCR analysis demonstrated that 1alpha,25(OH)2D3 and the synthetic PPARdelta ligand L783483 show a cell and time-dependent interference in each other's effects on VDR mRNA expression, so that their combined application shows complex effects on the induction of VDR target genes, such as CYP24. Taken together, we conclude that PPARdelta is a primary 1alpha,25(OH)2D3-responding gene and that VDR and PPARdelta signaling pathways are interconnected at the level of cross-regulation of their respective transcription factor mRNA levels.



    PreMedline Identifier: 15890193


    Now we have had other threads on Vitamin D and its striking neuro-trophic actions. It seems to stand out as a very useful, almost overlooked brain supporting nutrient.



    Vitamin D3 also raises calcium uptake so I'd take it away from calcium.



    Ibuprofen and NSAID's;




    Evaluation of human peroxisome proliferator-activated receptor (PPAR) subtype selectivity of a variety of anti-inflammatory drugs based on a novel assay for PPAR delta(beta).



    Drs. Paul Sternberg and Franco Recchia evaluate possible changes in ophthalmic practice with anti-VEGF agents; Dr. Paul Latkany presents an unusual case; Dr. Robert Bernardino reviews the literature.





    J Pharmacol Sci. 2003; 93(3):347-55 (ISSN: 1347-8613)

    Kojo H; Fukagawa M; Tajima K; Suzuki A; Fujimura T; Aramori I; Hayashi K; Nishimura S

    Advanced Technology Platform Research Laboratory, Fujisawa Pharmaceutical Co., Ltd.,Tsukuba, Ibaraki, Japan. kojo@biomarker.co.jp



    The nuclear receptor PPAR (peroxisome proliferator-activated receptor) has three subtypes named alpha, delta(beta), and gamma that may act as receptors for a range of compounds including antihyperglycaemic drugs, insulin sensitizers, and non-steroidal anti-inflammatory drugs (NSAIDs). Although profiling of the subtype selectivity of the compounds for PPAR is indispensable to elucidate their pharmacological action, the absence of an appropriate transactivation assay for PPAR delta led us to develop a sensitive and reproducible method. We found that co-expression of PPAR delta, retinoid X receptor (RXR) alpha, and coactivators such as CBP and SRC-1 enhanced basal and agonist-dependent activation of PPAR responsive element (PPRE)-driven transcription by PPAR delta, rendering a PPRE-driven reporter assay reliable and sensitive. Utilizing this assay for PPAR delta, we re-evaluated the subtype selectivity of a variety of anti-inflammatory drugs for human PPAR. The PPAR agonists tested included two leukotriene (LT) D(4) antagonist, seven NSAIDs, and two anti-rheumatoid drugs. We found that a novel LTD(4) antagonist, FK011 ([2-(((2-(4-tert-butyl-1,3-thiazol-2-yl)-1-benzofuran-5-yl)oxy)methyl)phenyl]acetic acid), showed marked agonistic activity for PPAR gamma. NSAIDs were classified into the following three groups: those showing no activity for all subtypes, those that were selective for PPAR gamma such as indomethacin and diclofenac, and those showing agonistic activity for the delta and gamma subtypes such as ibuprofen. These results will be important to studies on the molecular mechanisms of pharmacological actions of LTD(4) antagonists and NSAIDs.



    PreMedline Identifier: 14646253


    Unfortunately there are pros and cons of NSAID's like ibuprofen. I'd take it over statins however.



    Another reason to take your Omega 3’s is that they stimulate the receptor.






    (6) Inflammatory Mechanisms in Alzheimer’s Disease: Inhibition of b-Amyloid-Stimulated Proinflammatory Responses and Neurotoxicity by PPAR- Agonists



    Colin K. Combs, Derrick E. Johnson, J. Colleen Karlo, Steven B. Cannady, and Gary E. Landreth. Alzheimer Research Laboratory, Departments of Neurosciences and Neurology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106. The Hournal of Neuroscience, Jan 15 2000



    The research investigates that Nonsteroidal anti-inflammatory drugs (NSAIDs), drugs of the thiazolidinedione class, and the natural ligand prostaglandin J2 act as agonists for PPAR- and inhibit the b-amyloidstimulated secretion of proinflammatory products by microglia and monocytes responsible for neurotoxicity and astrocyte activation. The activation of PPAR- also arrested the differentiation of monocytes into activated macrophages. PPAR- agonists were shown to inhibit the b-amyloid-stimulated expression of the cytokine genes interleukin-6 and tumor necrosis factor a. Furthermore, PPAR- agonists inhibited the expression of cyclooxygenase-2. These data provide direct evidence that PPAR- plays a critical role in regulating the inflammatory responses of microglia and monocytes to b-amyloid. The research found the efficacy of NSAIDs in the treatment of AD may be a consequence of their actions on PPAR- rather than on their canonical targets the cyclooxygenases. Importantly, the efficacy of these agents in inhibiting a broad range of inflammatory responses suggests PPAR- agonists may provide a novel therapeutic approach to Alzeimer disease.


    Lowering IL-6 during the day is almost certainly going to be beneficial in reducing the neuro-inflammation associated with this condition. Normally IL-6 follows a diurnal rhythm peaking at night.



    At this point it may be essential for all round health. Sleep deprivation and other related conditions usually are marked by a pronounced increase in IL-6 during the day. DHEA helps to lower it, as does Vitamin K according to 2 studies. Vitamin K's actions in the brain are much less understood as it undergoes conversion to menaquinone, however there are ways actions on the 'periphery' which includes the cerebral vesels and the BBB, may make a strong atni-inflammatory role for Vitamin K in Alz. Although it is speculative, it at least appears to have multiple other benefits. Sleep of good quyality is very important to optimise function of microglia, which may assist removal of intra-cellular amyloid, and boost neuroprotective processes, and cell repair. Raising eNOS (an enzyme that makes Nitric Oxide) may be very beneficial and anti-inflammatory. The inflammation in ALZ very well could have a strong cause in vascular processes, and eNOS works that way in the endothelium. Ginkgo is reported to raise eNOS but lower iNOS which looks to be broadly beneficial, especially during the day. The other reported benefit of NO from the endothelium is increased stem cell production. Neurogenesis also happens specifically through low NO levels, which would be anticipated in deep sleep.



    So that gives me cause to explore those options. That should cover the main stuff for a whistle stop tour, we can explore a lot more later.
    ------



    These ideas are released under a Creative Commons Share and Share alike license

  7. #7
    Senior Member Squarepusher's Avatar
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    Quote Originally Posted by akp2004' post='373164' date='Nov 22 2006, 11:16 PM

    This community means much to me.

    I just talked with my mom.

    My dad''s 86 -- hiz mom died at 93 so not expecting early death. So, short of accepting we put him in a carefacility, what is the most up to date research and speculative resarch that focused or can keep early Alzheimer's stable for as long as possible.



    Pharmaceutical

    Nootropic/Alternative



    This is a huge pain in our family.



    I know this info is spread among the board in framenfs. i need a collective summary

    documented medical studies, and summarize current suggested treamtments, that i can presenf to my dad and his treatment team..



    I will pay for time invested in those who collect studies - my dad's a former research professor and is not going to take a recommendation like "galantamine has been shown to be helpful." I pay well for proper research.



    I will also donate money if that's not your driving force.



    Please - I need help - Mom is at breaking point, and anything is appreciated; I am working to the bone.

    Connecting to my dad intellectually was out main way of bonding - this is very painful



    I believe he was on Aricept (no change),now on Exelon (sp?)



    Please trust too, if I pay you, I will sign an NDA that has terms of non medical advice, or rewrite so it comes from me.. This is not an entrapment bullshit... Just reaching out for help, that crosses a bit into the disease treatment questions

    --please pm me or post in the thread.

    EDIT: Saturday morning --- I appreciate Klee and Eclypz's post. I think the money thing was motivated by sheer shock, and wanting a fast solution - I also know time is tight for alot of people. But thank you for your expression around community ethos around helping for the sake of helping.


    the only thing i heard recently, is marijuana apparently reduces inflammation associated with alzhtimers ...



    not that i use that stuff or trust the study ... i have heard some people claim modafinil may slow sognitive decline ... then as far as the otehr stuff you have all the supps, like ALCAR, NAC, -racetams, grape seed, you can look into ...



    also i think exercise is a good prevention, but im not sure thats a big option at the advanced 80's stage.



    so, sorry i couldn't be a big help, try ImmInst they have some good resources there.

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    You could try Imminst but you've got much of the important data right here. Can people also not repeat things and instead try to add data. Thanks.
    ------



    These ideas are released under a Creative Commons Share and Share alike license

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    Senior Member noos's Avatar
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    I would evaluate modafinil use, AFAIK its action is related to glutamate.



    This reminded me of memantine (a moderate affinity NMDA-receptor antagonist). Google or www.memantine.com



    And yes exercise is good (BDNF, GH, oxigenation, etc.) and there must be something for a 80 yrs old person.

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    I wouldn't take modifinal. The likelihood is that it will not benefit restorative sleep. Go back and look at PPAR delta and Vitmin D, niacinamide and the like.



    I would suggest that he try to get outside and walk in conjunction with morning light to help sleep and provide activity at the same time.
    ------



    These ideas are released under a Creative Commons Share and Share alike license

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    Senior Member Benson's Avatar
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    Quote Originally Posted by ATB' post='373419' date='Nov 25 2006, 11:37 AM

    I wouldn't take modifinal. The likelihood is that it will not benefit restorative sleep. Go back and look at PPAR delta and Vitmin D, niacinamide and the like.



    I would suggest that you try to get outside and walk in conjunction with morning light to help sleep and provide activity at the same time.


    ATB have you seen the data on nicotine? I'd be interested to hear your thoughts...
    Remember, believe none of what you hear and half of what you see...





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    Senior Member akp2004's Avatar
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    Quote Originally Posted by Benson' post='373421' date='Nov 25 2006, 10:00 AM

    ATB have you seen the data on nicotine? I'd be interested to hear your thoughts...




    Thank you to everyone's thorough replies, and summarizing huge amounts of info.



    Thanksgiving is tough enough - and when you see your dad decline, there's nothing more painful, especially when the main connection between us was intellectual -- college professor dad, son making his way thru college and grad school as our adult connection.



    Again, thank you for your replies and help,





    A

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    Senior Member razg's Avatar
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    Quote Originally Posted by akp2004' post='373565' date='Nov 26 2006, 10:30 PM

    Thank you to everyone's thorough replies, and summarizing huge amounts of info.



    Thanksgiving is tough enough - and when you see your dad decline, there's nothing more painful, especially when the main connection between us was intellectual -- college professor dad, son making his way thru college and grad school as our adult connection.



    Again, thank you for your replies and help,

    A


    I'd wager your dad is pretty aware and proud of the way that you have chosen to go around taking charge of the situation, regardless of his condition.
    <span style="font-size:10pt;line-height:100%">Power is realising your strength, inner strength, controlling yourself.</span>

    <span style="font-size:10pt;line-height:100%">"Fall seven times, stand up eight." - Japanese proverb</span>

    <span style="font-size:14pt;line-height:100%">IronArena.com</span>

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    Linked below is a thread to an older thread here,seeking advice on treating Alzheimer's.



    Acupuncture was mentioned and ScottL posted a few studies indicating choline as a promising adjunct to a treatment regimin:



    http://www.mindandmuscle.net/forum/index.p...pid=373553&



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    Yeah, choline and alcar are good additions, but as part of wider changes.



    As for Vitamin D3 and Omega 3's, I'd consider 1+g of EPA, 500mg+ DHA, and 1000iu+ of Vitamin D3.



    Even if the stimulant effect of D3 on PPAR delta doesn't work out for everyone, elderly people are frequently deficient, and it also helps bones. If he is deficient, chances are improved that it will support brain health and reduce the inflammation of the Alz condition, in a number of ways.



    Cod Liver Oil is one option.
    ------



    These ideas are released under a Creative Commons Share and Share alike license

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    has a Ketogenic diet already been mentioned?
    Just because I do not want something to happen -- does not mean that I need to fear it.

    Anxiety is just a tool that one uses in times of uncertainty. There are many other tools readily available that one would be better off learning to use.

    What is the greatness of man -- other than unjust classifications and imbalanced optimizations?

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    Also I posted on Scyllo-inositol (sp?) a while back. Probably next to impossible to get, and still not much would be known wrt overall safety. I think that it may exert its effect through changes in the way that glucose is handled... but that is all speculation on my part.
    Just because I do not want something to happen -- does not mean that I need to fear it.

    Anxiety is just a tool that one uses in times of uncertainty. There are many other tools readily available that one would be better off learning to use.

    What is the greatness of man -- other than unjust classifications and imbalanced optimizations?

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    Are there any issues with 1000iu+ of Vitamin D3 per day for a healthy person?



    ATB and others great posts!



    Scyllo-inositol and curcumin seem very interesting...
    To cut the Gordian knot.

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    Quote Originally Posted by kLee' post='374114' date='Nov 29 2006, 12:12 AM

    Are there any issues with 1000iu+ of Vitamin D3 per day for a healthy person?


    Just saw this: http://www.mindandmuscle.net/forum/i...howtopic=26361
    To cut the Gordian knot.

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    Quote Originally Posted by Logos' post='373891' date='Nov 28 2006, 01:25 AM

    has a Ketogenic diet already been mentioned?
    thats interesting since i heard some scientists were saying alz might actually by a sort of type-3 diabetes. insulin related, so of course cutting grains/sugar might be intersting.

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