Lipofuscin Options

[piet3r]

I'm wondering if someone can give me a list of nutrients that prevent/help against lipofuscin.

I'm aware of the following:

Acetyl-l-carnitine
Lipoic acid
DMAE (some indicate only Centrophenoxine helps against lipofuscin, whilst others state DMAE does as well)

Since there is confusion on DMAE I'm wondering about incorporating other possible nutrients. I take high dose carnosine for preventing glycation and lipofuscin seems to be the only gap in carnosine's protection.


Any help is appreciated.

[kclo4x]

I'm wondering if someone can give me a list of nutrients that prevent/help against lipofuscin.

I'm aware of the following:

Acetyl-l-carnitine
Lipoic acid
DMAE (some indicate only Centrophenoxine helps against lipofuscin, whilst others state DMAE does as well)

Since there is confusion on DMAE I'm wondering about incorporating other possible nutrients. I take high dose carnosine for preventing glycation and lipofuscin seems to be the only gap in carnosine's protection.


Any help is appreciated.

"Piracetam appears to reduce levels of lipofuscin in the rat brain.^[21] (Lipofuscin accumulation is common symptom of aging and alcoholism)." - wiki

http://www.blackwell-synergy.com/doi/abs/1...ournalCode=acer

[stephen_b]

I was surprised by the amount of lipofuscin accumulation in the speech areas of the brain in the study "A Microscopic Study of Language-Related Cortex in Autism" (abstract, full text):

In controls, the number of lipofuscin containing cells in full-depth cortical samples increased
in all three brain areas from age 8 to age 56 in area 22 by 770% (p = 0.0015); area 39 by 430%
(p = 0.0001); and from age 8 to age 46 in area 44 by 189% (p = 0.0001).

That doesn't sound good. I've started taking 800 mg of piracetam daily. Anyone know whether lipofuscin accumulation impacts other parts of the body?

StephenB

[piet3r]

Funny coincidence, u have revived this thread, and 10 minutes before seeing it again, I stumbled upon this link:

http://www.ergo-log.com/creatinelongevity.html

"When brains – and not only brains – age, the amount of the ‘aging pigment’ lipofuscin in the brain tissue increases. Lipofuscin is therefore a marker for aging. The Germans discovered that the hippocampus of the mice in the creatine group contained less lipofuscin. ".

So that basically answers the question that it's not only in the brain, but also that there's another compound to add to this thread/list, which is creatine, also useful against lipofuscin.

U should also go for the Centrophenoxine.

[luv2increase]

DMAE does not remove lipofuscin. It needs to be combined to the plant hormone PCA which makes centrophenoxine for this to occur.



http://www.ncbi.nlm.nih.gov/sites/entrez

1: Exp Aging Res. 1978 Apr;4(2):133-9.Links
Effects of PCA and DMAE on the namatode Caenorhabditis briggsae.
Zuckerman BM, Barrett KA.

Concentration of 6.8 mM DMAE did not retard age pigment accumulation in Caenorhabditis briggsae. However, when the nematodes were exposed to 6.8 mM PCA + 6.8 mM DMAE combined, the accumulation of age pigment was significantly retarded. A combination of 3.4 mM DMAE + 3.4 mM PCA had no effect on age pigment. It is concluded from this study that PCA and DMAE act in concert to produce the observed effect on age pigment. In respect to this parameter neither molecule was effective alone. The results indicate that the effect of centrophenoxine on age pigment might be enhanced by retarding the hydrolysis of centrophenoxine. The accumulation of electron dense aggregates, thought to be aggregates of cross-linked molecules, was reduced by 6.8 PCA + 6.8 DMAE. It is suggested that centrophenoxine be tested for its ability to remove random, unwanted cross-linkages in higher animals.

PMID: 348477 [PubMed - indexed for MEDLINE]

[caston]

So what does PCA stand for?

[frankbuzin]

So what does PCA stand for?

Perchloric Acid

[caston]

http://en.wikipedia.org/wiki/Perchloric_acid

Hardly looks like a safe supplement...

[frankbuzin]

http://en.wikipedia.org/wiki/Perchloric_acid

Hardly looks like a safe supplement...

Well does "pyrrolidone carboxylic acid" look better? J/K

No seriously Caston... I apologize... I should have looked at what you were discussing closer as neither are what you are really after. In the context of Centrophenoxine it is actually Parachlorophenoxyacetate (also often referred to as pCPA)

This post has been edited by frankbuzin: Mar 7 2009, 10:25 AM

[caston]

http://en.wikipedia.org/wiki/Perchloric_acid

Hardly looks like a safe supplement...

Well does "pyrrolidone carboxylic acid" look better? J/K

No seriously Caston... I apologize... I should have looked at what you were discussing closer as neither are what you are really after. In the context of Centrophenoxine it is actually Parachlorophenoxyacetate (also often referred to as pCPA)

Thank you

[krillin]

According to Aubrey's book, centrophenoxine doesn't work either. It seems that people were mistakenly calling ceroid lipofuscin. Here are some of what he cites.

Ann N Y Acad Sci. 2002 Apr;959:57-65.
Pigments in aging: an overview.
Porta EA.
Department of Pathology, University of Hawaii, School of Medicine, Honolulu, Hawaii 96822, USA. portae@jabsom.biomed.hawaii.edu

Although during the normal aging process there are numerous pigmentary changes, the best recognized are those of melanin and lipofuscin. Melanin may increase (e.g., age spots, senile lentigo, or melanosis coli) or decrease (e.g., graying of hair or ocular melanin) with age, while lipofuscin (also called age pigment) always increases with age. In fact, the time-dependent accumulation of lipofuscin in lysosomes of postmitotic cells and some stable cells is the most consistent and phylogenetically constant morphologic change of aging. This pigment displays a typical autofluorescence (Ex: approximately 440; Em: approximately 600 nm), sudanophilia, argyrophilia, PAS positiveness, and acid fastness. Advances on its biogenesis, composition, evolution, and lysosomal degradation have been hampered by the persistent confusion between lipofuscin and the large family of ceroid pigments found in a variety of pathological conditions, as evidenced by the frequent use of the hybrid term lipofuscin/ceroid by investigators mainly working with in vitro systems of disputable relevance to in vivo lipofuscinogenesis. While lipofuscin and ceroid pigments may share some of their physicochemical properties at one moment or another in their evolutions, these pigments have different tissue distribution, rates of accumulation, origin of their precursors, and lectin binding affinities. Although it is widely believed that lipofuscin is a marker of oxidative stress, and that it can be, therefore, modified by antioxidants and prooxidants, these assumptions are mainly based on in vitro experiments and are not generally supported by in vivo studies. Another common misconception is the belief that lipofuscin can be extracted from tissues by lipid solvents and measured spectrofluorometrically. These and other disturbing problems are reviewed and discussed in this presentation.

PMID: 11976186

Exp Gerontol. 1985;20(6):333-40.
Quantitative studies of the effects of aging, meclofenoxate, and dihydroergotoxine on intraneuronal lipopigment accumulation in the rat.
Dowson JH.

Intraneuronal lipopigment accumulation is associated with ageing and certain diseases, and there are many claims that this can be influenced by drugs, particularly meclofenoxate (centrophenoxine). The various unsubstantiated or conflicting reports of the effects of this drug in animal studies indicate the need for methods for the demonstration of lipopigment accumulation in adequately defined, easily-identified, and relatively homogeneous neuronal populations; this study has validated two such methods by demonstrating significant differences between groups of rats at different ages in respect of measured lipopigment autofluorescence intensity from the most heavily pigmented regions of a subpopulation of Purkinje cells, and of the area overlying intraneuronal lipopigment in a region of the hippocampus. These methods were then used to investigate the effects of daily (5 days per week) intraperitoneal injections of meclofenoxate or dihydroergotoxine, over a period of 12 weeks, before sacrifice at 13.5 months. No significant effects of meclofenoxate were detected, but dihydroergotoxine administration was associated with a significant increase in mean area overlying intraneuronal lipopigment in the CA3a region of the hippocampus. The results do not confirm that meclofenoxate can induce a reduction in intraneuronal lipopigment, but suggest that chronic dihydroergotoxine administration was associated with an increase in intraneuronal volume of lipopigment in the cell bodies of CA3a hippocampal neurones.

PMID: 3938737

Neurobiol Aging. 1986 Mar-Apr;7(2):107-13.
Lipofuscin in retinal pigment epithelium of rhesus monkey: lack of diminution with centrophenoxine treatment.
Andrews LD, Brizzee KR.

An experiment was performed to test the ability of Centrophenoxine to reduce the amount of lipofuscin (age pigment) in the retinal pigment epithelium (RPE) of aged rhesus monkeys. Centrophenoxine is reputed to have this action in neurons of lower mammals. Quantitative electron microscopic analysis was performed on sections from the perifovea of ten rhesus monkeys, all approximately 20 years of age. Four of the animals received 80 mg/kg Centrophenoxine (IM injection) daily for 12 weeks. No significant difference between the treated and control groups could be demonstrated statistically (Mann-Whitney U-test) either in the fraction of RPE cell cytoplasm occupied by lipofuscin granules or in the average size of the granules.

PMID: 3083280

J Gerontol. 1983 Sep;38(5):525-31.
Lipofuscin response to the "aging-reversal" drug centrophenoxine in rat retinal pigment epithelium and frontal cortex.
Katz ML, Robison WG Jr.

The effects of centrophenoxine on the lipofuscin contents of the retinal pigment epithelium (RPE) and frontal cortex of the brain were examined in senescent female Fischer rats. Rats (106 weeks old) were injected daily for 11 weeks with centrophenoxine (80 to 120 mg/kg body weight) or saline, and then sacrificed along with untreated 28- and 46-week-old controls. The number of lipofuscin granules seen in the RPE by light microscopy increased by 70% between 28 and 117 weeks of age in control animals. There was a concomitant age-related increase in lipofuscin specific fluorescence in the RPE. Centrophenoxine treatment neither reduced the amount of lipofuscin, nor altered the ultrastructural appearance of lipofuscin granules in the RPE. Between 28 and 117 weeks of age, there was an almost nine-fold increase in the lipofuscin content of the frontal cortex of control animals; centrophenoxine treatment failed to reverse this pigment accumulation.

PMID: 6411800

[piet3r]

Very interesting krillin. But does he mention a method that we CAN use?

First debunking MK-4 and now this. Sure saves me a couple of bucks, for that I thank you .

[waldemar]

F**k. Ok, no more Centrophenoxine for me... Or is there something else that it's good for (except as a Choline source)?

[krillin]

Very interesting krillin. But does he mention a method that we CAN use?

Nope. That's why we need LysoSENS.

[waldemar]

Ok, what about ALCAR?

[luv2increase]

I wouldn't take in those studies posted for centrophenoxine's inability of lipofuscin removal and prevention for granted. There are more studies which show it does a great job at doing so. It is more so a majority pull if you know what I mean.

[krillin]

I wouldn't take in those studies posted for centrophenoxine's inability of lipofuscin removal and prevention for granted. There are more studies which show it does a great job at doing so. It is more so a majority pull if you know what I mean.

As I noted, the authors of the positive studies were actually studying something else that they erroneously called lipofuscin.

[luv2increase]

I wouldn't take in those studies posted for centrophenoxine's inability of lipofuscin removal and prevention for granted. There are more studies which show it does a great job at doing so. It is more so a majority pull if you know what I mean.

As I noted, the authors of the positive studies were actually studying something else that they erroneously called lipofuscin.

Hmmm.. You quoted According to Aubrey's book, centrophenoxine doesn't work either. It seems that people were mistakenly calling ceroid lipofuscin. Here are some of what he cites.. This could be taken as two different meanings. 1) We were wrong because we thought centrophenoxine was removing was lipofuscin, but it indeed was ceroid instead, or 2) The studies you posted were referring to the erroneous lipofuscin and not the real deal hence they don't have any meaning because they show centrophenoxine isn't effective against ceroid rather than lipofuscin.


I think you need to be a little more specific. It should have been a warning sign to you krillin that you were being misunderstood when waldemar posted

F**k. Ok, no more Centrophenoxine for me... Or is there something else that it's good for (except as a Choline source)?

.... I guess it needed more than one person for you to understand you were being misunderstood. Oh well, at least we know that centrophenoxine is all good now for the REAL lipofuscin.

Cheers

[VespeneGas]

Not to speak for Krillin, but I read his comment as unambiguously (1), that centrophenoxine reduces a pigment other than lipofuscin. I'm not sure how waldemar's comment is evidence of confusion, only that centrophenoxine doesn't do what it has historically purported to do, and therefore isn't worth the price (if it's just a fancy choline source).

[piet3r]

It seemed pretty clear to me that he showed that it's not worth taking centrophenoxine if for the purpose of lowering lipofuscin content in the brain. That was the only reason I was taking it. Indeed, it seems that it's purpose is more an expensive DMAE/choline supplement. DMAE wasn't a good source for choline as I remember reading something that it competed with other choline sources in the brain (don't quote me), and therefore phosphatidylcholine, alpha-gpc, are the better forms to stick with. Choline bitartrate is a no go, and I'm still wondering whether PPC is actually equivalent to alpha-gpc:

http://www.lef.org/Vitamins-Supplements/It.../HepatoPro.html

http://www.lef.org/magazine/mag2000/mar00-report.html

http://www.lef.org/magazine/mag2005/jul2005_aas_01.htm

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