Low cerebral vitamin B5 pantothenic acid as a reversible possible cause of neurodegeneration & dementia in Alzheimers Huntingtons Parkinsons [myelin]

[cs3000]

Cerebral Vitamin B5 (D-Pantothenic Acid) Deficiency as a Potential Cause of Metabolic Perturbation and Neurodegeneration in Huntington’s Disease​

Huntingtons disease,

Cerebral Vitamin B5 (D-Pantothenic Acid) Deficiency as a Potential Cause of Metabolic Perturbation and Neurodegeneration in Huntington’s Disease - PMC

Huntington’s disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in exon 1 of the HTT gene. HD usually manifests in mid-life with loss of GABAergic projection neurons from the striatum accompanied by progressive atrophy of ...

www.ncbi.nlm.nih.gov

Alzheimers disease

Cerebral deficiency of vitamin B5 (d-pantothenic acid; pantothenate) as a potentially-reversible cause of neurodegeneration and dementia in sporadic Alzheimerâs disease

Alzheimer’s disease (AD) is the most common cause of age-related neurodegeneration and dementia, and there are no available treatments with proven dis…

www.sciencedirect.com

*Pantothenic acid exists at higher concentrations in the brain relative to in blood, being about [10 fold to] 50-fold higher
We found that widespread, severe cerebral deficiency of vitamin B5 occurs in AD. This deficiency was worse in those regions known to undergo severe damage, including the hippocampus, entorhinal cortex, and middle temporal gyrus.

In brain, acetyl-CoA is the obligate precursor of the neurotransmitter acetylcholine, and the complex fatty-acyl groups that mediate the essential insulator role of myelin, both processes being defective in AD; moreover, the large cerebral vitamin B5 concentrations co-localize almost entirely to white matter. Vitamin B5 is well tolerated when administered orally to humans and other mammals.

We conclude that cerebral vitamin B5 deficiency may well cause neurodegeneration and dementia in AD, which might be preventable or even reversible in its early stages, by treatment with suitable oral doses of vitamin B5.

Parkinsons disease
Substantively Lowered Levels of Pantothenic Acid (Vitamin B5) in Several Regions of the Human Brain in Parkinson’s Disease Dementia

It has previously been shown that pantothenic acid is significantly decreased in multiple brain regions in both Alzheimer’s disease (ADD) and Huntington’s disease (HD). The current investigation aimed to determine whether similar changes are also present in cases of Parkinson’s disease dementia (PDD), another age-related neurodegenerative condition, and whether such perturbations might occur in similar regions in these apparently different diseases.

Brain tissue was obtained from nine confirmed cases of PDD and nine controls with a post-mortem delay of 26 h or less. Tissues were acquired from nine regions that show high, moderate, or low levels of neurodegeneration in PDD: the cerebellum, motor cortex, primary visual cortex, hippocampus, substantia nigra, middle temporal gyrus, medulla oblongata, cingulate gyrus, and pons.

A targeted ultra–high performance liquid chromatography—tandem mass spectrometry (UHPLC-MS/MS) approach was used to quantify pantothenic acid in these tissues. Pantothenic acid was significantly decreased in the cerebellum (p = 0.008), substantia nigra (p = 0.02), and medulla (p = 0.008) of PDD cases. These findings mirror the significant decreases in the cerebellum of both ADD and HD cases, as well as the substantia nigra, putamen, middle frontal gyrus, and entorhinal cortex of HD cases, and motor cortex, primary visual cortex, hippocampus, middle temporal gyrus, cingulate gyrus, and entorhinal cortex of ADD cases. Taken together, these observations indicate a common but regionally selective disruption of pantothenic acid levels across PDD, ADD, and HD.

b5 plays a key role in age related cognitive decline , as it's used for myelin / white matter. Myelin = the sheath around nerves that enables electrical signals to travel well. also b5 is needed for acetyl-coa, for cellular ATP / oxidative phosphorylation / mitochondria function
Vitamin B5 (d-pantothenic acid) localizes in myelinated structures of the rat brain: Potential role for cerebral vitamin B5 stores in local myelin homeostasis

We recently found that cerebral pantothenate is markedly lowered, averaging ∼55% of control values in cases of Huntington's disease (HD) including those who are pre-symptomatic, and that regions where pantothenate is lowered correspond to those which are more severely damaged

Remarkably, cerebral pantothenate was almost entirely localized to myelin-containing structures in both experimental groups

These findings are consistent with physiological localization of pantothenate in myelinated white-matter structures, where it could serve to support myelin synthesis. Further investigation of cerebral pantothenate is warranted in neurodegenerative diseases such as HD and Alzheimer's disease, where myelin loss is a known characteristic of pathogenesis.

theres a correlation with higher mortality for people that have high blood pressure with high b5 Association between plasma Vitamin B5 levels and all‐cause mortality: A nested case‐control study but its not an intervention study, so the correlation doesnt prove the b5 as a cause. but maybe something worth looking into with high blood pressure to work out whats going on there. Effect of Pantethine on Ovarian Tumor Progression and Choline Metabolism Immunostimulatory effects of vitamin B5 improve anticancer immunotherapy its anti-cancer (pro immunity)

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So low cerebral pantothenic acid may be a primary cause of alzheimers , huntingtons, parkinsons dementia, and general age related cognitive decline. and boosting intake of B5 taken by itself away from other b vitamins https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1471-4159.1986.tb00705.x especially biotin, which reduces the amount of b5 that crosses the blood brain barrier into the brain, may be a nice help for cognition in older age

 

[Johann2547]

Is there a particular form of B5 that is best?

 

[cs3000]

@Johann2547 not sure but ray thought pantothenic acid is generally pretty safe to take, and said can go up to 100mg - 200mg occasionally

an intervention study using pantethine (metabolises to pantothenic aicd), in Alzheimers model
https://link.springer.com/article/10.1007/s13311-019-00754-z

We observed that long-term pantethine treatment significantly reduced glial reactivity and Αβ deposition, and abrogated behavioral alteration in Tg mice. Moreover, the transcriptomic profiles revealed that after pantethine treatment, the expression of genes differentially expressed in Tg mice, and in particular those known to be related to AD, were significantly alleviated.

Altogether, our data support a beneficial role for long-term pantethine treatment in preserving CNS crucial functions altered by Aβ pathogenesis in Tg mice and highlight the potential efficiency of pantethine to alleviate AD pathology. (maybe used ~3000mg human dose 3x a week, has to be converted to pantothenic acid in intestine so assuming would be lower dose for pantothenic acid)

 

[Johann2547]

I tried Pantethine several years ago and would notice an immediate boost of some sort in the brain. Not all pantethine is of good quality. The brand I was using was Source Naturals. It boosted BDNF. Also, it helps to remove aldehydes.

 

[Scuppi]

I was always intrigued by pantethine, and wondered if it would be useful to use as a supplement, due to its CoA increasing effect. I used it years ago, then pretty much forgot about it, since my b complex has b-5 in it. It may warrant revisiting, if nothing else, to see if there is any new research on it.

 

[OLLNX]

Cerebral Vitamin B5 (D-Pantothenic Acid) Deficiency as a Potential Cause of Metabolic Perturbation and Neurodegeneration in Huntington’s Disease​

Huntingtons disease,

Cerebral Vitamin B5 (D-Pantothenic Acid) Deficiency as a Potential Cause of Metabolic Perturbation and Neurodegeneration in Huntington’s Disease - PMC

Huntington’s disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in exon 1 of the HTT gene. HD usually manifests in mid-life with loss of GABAergic projection neurons from the striatum accompanied by progressive atrophy of ...

www.ncbi.nlm.nih.gov

Alzheimers disease

Cerebral deficiency of vitamin B5 (d-pantothenic acid; pantothenate) as a potentially-reversible cause of neurodegeneration and dementia in sporadic Alzheimerâs disease

Alzheimer’s disease (AD) is the most common cause of age-related neurodegeneration and dementia, and there are no available treatments with proven dis…

www.sciencedirect.com

Parkinsons disease
Substantively Lowered Levels of Pantothenic Acid (Vitamin B5) in Several Regions of the Human Brain in Parkinson’s Disease Dementia




b5 plays a key role in age related cognitive decline , as it's used for myelin / white matter. Myelin = the sheath around nerves that enables electrical signals to travel well. also b5 is needed for acetyl-coa, for cellular ATP / oxidative phosphorylation / mitochondria function
Vitamin B5 (d-pantothenic acid) localizes in myelinated structures of the rat brain: Potential role for cerebral vitamin B5 stores in local myelin homeostasis




theres a correlation with higher mortality for people that have high blood pressure with high b5 Association between plasma Vitamin B5 levels and all‐cause mortality: A nested case‐control study but its not an intervention study, so the correlation doesnt prove the b5 as a cause. but maybe something worth looking into with high blood pressure to work out whats going on there. Effect of Pantethine on Ovarian Tumor Progression and Choline Metabolism Immunostimulatory effects of vitamin B5 improve anticancer immunotherapy its anti-cancer (pro immunity)

-
So low cerebral pantothenic acid may be a primary cause of alzheimers , huntingtons, parkinsons dementia, and general age related cognitive decline. and boosting intake of B5 taken by itself away from other b vitamins https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1471-4159.1986.tb00705.x especially biotin, which reduces the amount of b5 that crosses the blood brain barrier into the brain, may be a nice help for cognition in older age

Interesting. Thanks for posting!

 

[shell_inspector]

Will large doses of B5 cause resistance or withdrawal symptoms? People taking high doses B3 get an energy crash after few months of heavy dosing.

 

[cs3000]

Will large doses of B5 cause resistance or withdrawal symptoms? People taking high doses B3 get an energy crash after few months of heavy dosing.

no resistance or withdrawal but there is a link to more cortisol+progesterone production in the adrenals from b5 at high dose like 1g. i tried high dose short term to see if i noticed a cortisol effect but i didnt notice much. some people see more hair loss on high doses maybe because of that long term. but maybe a lower dose ~ 100mg could be enough for the cognition / myelin restoring effect over time without this