Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, May 12, 2020

Proton pump inhibitors act with unprecedented potencies as inhibitors of the acetylcholine biosynthesizing enzyme—A plausible missing link for their association with incidence of dementia

You are already under high risk of getting dementia. What the fuck is your doctor EXACTLY doing to prevent that? This prevention is your doctor's responsibility, don't let them weasel out of it. You should get EXACT PROTOCOLS ON PREVENTION. Don't settle for crapola guidelines like the Mediterranean diet, that barely helps because there is no specificity to it.

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

5. Parkinson’s Disease May Have Link to Stroke March 2017

 

 

Proton pump inhibitors (PPIs) are a class of drugs used to treat GERD, peptic ulcers, and H. pylori.

The currently available PPIs include:

  • omeprazole (Prilosec, Prilosec OTC, Zegerid)

  • lansoprazole (Prevacid)

  • pantoprazole (Protonix)

  • rabeprazole (Aciphex)

  • esomeprazole (Nexium)

  • dexlansoprazole (Dexilant)

  

Proton pump inhibitors act with unprecedented potencies as inhibitors of the acetylcholine biosynthesizing enzyme—A plausible missing link for their association with incidence of dementia


First published: 08 May 2020






Abstract




Introduction

Several pharmacoepidemiological studies indicate that proton pump inhibitors (PPIs) significantly increase the risk of dementia. Yet, the underlying mechanism is not known. Here, we report the discovery of an unprecedented mode of action of PPIs that explains how PPIs may increase the risk of dementia.

Methods

Advanced in silico docking analyses and detailed enzymological assessments were performed on PPIs against the core‐cholinergic enzyme, choline‐acetyltransferase (ChAT), responsible for biosynthesis of acetylcholine (ACh).

Results

This report shows compelling evidence that PPIs act as inhibitors of ChAT, with high selectivity and unprecedented potencies that lie far below their in vivo plasma and brain concentrations.

Discussion

Given that accumulating evidence points at cholinergic dysfunction as a driving force of major dementia disorders, our findings mechanistically explain how prolonged use of PPIs may increase incidence of dementia. This call for restrictions for prolonged use of PPIs in elderly, and in patients with dementia or amyotrophic lateral sclerosis.

1 INTRODUCTION

The cholinergic system is one of the oldest and the most widely spread neuronal and non‐neuronal signaling systems in the body, and in an evolutionary perspective has acquired regulatory functions in diverse biological processes and organs. The cholinergic neurons and their projections are identified by intracellular presence of the acetylcholine (ACh) bio‐synthesizing enzyme, choline‐acetyltransferase (ChAT). All other downstream neurons and non‐excitable cells which express ACh‐receptors are cholinoceptive cells. The central cholinergic system consists of four “ChAT‐containing” neuronal nuclei (Ch1–Ch4) located in the basal forebrain.1 Ch1 and Ch2 innervate the hippocampal complex, Ch3 the olfactory bulb. Ch4‐neurons are located in the nucleus basalis of Meynert (nbM), which innervate the rest of cerebral cortex and amygdala.1 These cholinergic nuclei and their widespread projections throughout the brain have recently been mapped in detail as a 3D whole‐brain atlas together with the morphology and the connectivity of individual neurons from the basal forebrain.2 In addition, extensive cholinergic neuronal projections, originated from 13 cranial nerves (CN0 and I‐XII, constituting the parasympathetic system3), reach throughout the body, thereby controlling autonomic function of diverse organs, muscles, and glands.4, 5 Another major neuronal system with extensive cholinergic circuitry is the enteric nervous system (ENS), in which about 64% of the neurons are cholinergic.6

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