Cerebral vitamin B5 deficiency (pantothenic acid) as a potentially reversible cause of neurodegeneration and dementia in Alzheimers HD PD [myelin]

[cs3000]

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

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 ...

www.ncbi.nlm.nih.gov

*Pantothenic acid exists at higher concentrations in the brain relative to plasma, 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.

b5 plays a role in helping age related cognitive decline , used for myelin aka. the sheath around nerves that enables electrical signals to travel well , along with cellular ATP from oxidative phosphorylation
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 in higher mortality for people that have high blood pressure 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 yet. it could be 1. they have higher b5 levels because they're taking a bunch of supplements & herbs to try and fix their hypertension and one of these or additives is creating the increased mortality risk 2. its actually the b5 by some mechanism [was thinking possibly the increase in oxphor ATP comes with more ROS, which increases oxidative stress burden without enough protection & reacts with pufa etc, but pantothenic acid increases glutathione if they were taking enough to counter that]. Effect of Pantethine on Ovarian Tumor Progression and Choline Metabolism Immunostimulatory effects of vitamin B5 improve anticancer immunotherapy it is anti-cancer and 3. something else


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.

low cerebral pantothenic acid intake 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 help

 

[moa]

@cs3000 yes, B5 was a major improvement when i discovered i have low acetylcholine.

was caused by low zinc but B5 supplements were very very strong. i took huge dose in the beginning 500mg B5 before sleep. i had very improved sleep with lots of dreams but woke up not feeling that good. went out to buy some food and i was feeling so bad i thought i was going to pass out or die.

felt better next day. i repeated this again with b5 500mg and DMAE, same thing but less strong not feeling like i was going to die this time. Then i took again but it kept decreasing the severity of the symptoms finally i bought 50mg pills and they are much better without side effects.

anyway, just to say it can have huge huge huge effect on the nerves and brain, autonomous system and vagal nerve tone in people who have low acetylcholine synthesis, and/or long term low zinc.

 

[Highserotonin90]

@moa Interesting so zinc is related to B5

 

[TruffleGnocchi]

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

Would be good to know if the brain is damaged because of lack of pantothenic acid, or is it that pantothenic acid is low, because there is less structure to store it