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peroxynitrite scavengers treat Alzheimer's disease
Serenoa
Posted: Thursday, September 1, 2016 5:20 AM
Joined: 4/24/2012
Posts: 484


Ok, starting to get a grasp on this. I see that high levels of myo-inositol are common in diabetes and metabolic syndrome:

"Myo-inositol (MI) converts into D-chiro-inositol (DCI) at rates that are specific for various types of tissues. However, MI to DCI conversion has been found to be much lower than normal in patients with type 2 diabetes (T2D) or PCOS, as evidenced by their measurement in blood, tissues and urine. For example, one study assessed the urinary ratio of MI/DCI in various populations and the results were as follows: 2.5 for control subjects; 20.4 for type 2 diabetic patients which may include PCOS patients."

https://cdn.shopify.com/s/files/1/0870/5152/files/Inositol_Modulation_of_Pathways_of_Insulin_Resistance-MetSyn-PCOS_and_T2DM-Paul_C-Brady_D-Townsend_Letter_9-2015.pdf

Also, I see that the breakdown of PIP2 leads to production of myo-inositol, and myo-inositol is then used in the process of creating phosphotidal inositols like PIP2 and PIP3. So it looks like too much myo-inositol may be indicative of two malfunctions: insulin resistance (as indicated above) and loss of PIP2 in the cell membrane (excessive PIP2 breakdown). 

Thank you Lane for the info and figures. I have much more to read on this. Since I'm not making the peroxynitrate connection yet, I can post further on this under another topic. I think there is an old Myo-inositol Topic somewhere.

 

 


Serenoa
Posted: Tuesday, October 25, 2016 5:49 AM
Joined: 4/24/2012
Posts: 484


An interesting connection to peroxynitrites...

 Arginine homeostasis in allergic asthma

"decreased NO synthesis and increased peroxynitrite formation"

Abstract

Allergic asthma is a chronic disease characterized by early and late asthmatic reactions, airway hyperresponsiveness, airway inflammation and airway remodelling. Changes in l-arginine homeostasis may contribute to all these features of asthma by decreased nitric oxide (NO) production and increased formation of peroxynitrite, polyamines and l-proline. Intracellular l-arginine levels are regulated by at least three distinct mechanisms: (i) cellular uptake by cationic amino acid (CAT) transporters, (ii) metabolism by NO-synthase (NOS) and arginase, and (iii) recycling from l-citrulline. Ex vivo studies using animal models of allergic asthma have indicated that attenuated l-arginine bioavailability to NOS causes deficiency of bronchodilating NO and increased production of procontractile peroxynitrite, which importantly contribute to allergen-induced airway hyperresponsiveness after the early and late asthmatic reaction, respectively. Decreased cellular uptake of l-arginine, due to (eosinophil-derived) polycations inhibiting CATs, as well as increased consumption by increased arginase activity are major causes of substrate limitation to NOS. Increasing substrate availability to NOS by administration of l-arginine, l-citrulline, the polycation scavenger heparin, or an arginase inhibitor alleviates allergen-induced airway hyperresponsiveness by restoring the production of bronchodilating NO. In addition, reduced l-arginine levels may contribute to the airway inflammation associated with the development of airway hyperresponsiveness, which similarly may involve decreased NO synthesis and increased peroxynitrite formation. Increased arginase activity could also contribute to airway remodelling and persistent airway hyperresponsiveness in chronic asthma via increased synthesis of l-ornithine, the precursor of polyamines and l-proline. Drugs that increase the bioavailability of l-arginine in the airways – particularly arginase inhibitors – may have therapeutic potential in allergic asthma.


Lane Simonian
Posted: Tuesday, October 25, 2016 9:50 AM
Joined: 12/12/2011
Posts: 5158


Here is a similar study:

Arginase Inhibition Restores Peroxynitrite-Induced Endothelial Dysfunction via L-Arginine-Dependent Endothelial Nitric Oxide Synthase Phosphorylation.

PURPOSE:

Peroxynitrite plays a critical role in vascular pathophysiology by increasing arginase activity and decreasing endothelial nitric oxide synthase (eNOS) activity. Therefore, the aims of this study were to investigate whether arginase inhibition and L-arginine supplement could restore peroxynitrite-induced endothelial dysfunction and determine the involved mechanism.

CONCLUSION:

These findings may explain the beneficial effect of arginase inhibition and L-arginine supplement on endothelial dysfunction under redox imbalance-dependent pathophysiological conditions.

A somewhat related problem is that the oxidation of BH4 by peroxynitrite leads to the formation of more peroxynitrite.


Within the central nervous system, tetrahydrobiopterin (BH4) is an essential cofactor for dopamine and serotonin synthesis. In addition, BH4 is now established to be an essential cofactor for all isoforms of nitric oxide synthase (NOS). Inborn errors of metabolism affecting BH4 availability are well documented and the clinical presentation can be attributed to a paucity of dopamine, serotonin, and nitric oxide (NO) generation. In this article, we have focussed upon the sensitivity of BH4 to oxidative catabolism and the observation that when BH4 is limiting some cellular sources of NOS may generate superoxide whilst other BH4 saturated NOS enzymes may be generating NO. Such a scenario could favor peroxynitrite generation. If peroxynitrite is not scavenged, e.g., by antioxidants such as reduced glutathione, irreversible damage to critical cellular enzymes could ensue. Such targets include components of the mitochondrial electron transport chain, alpha ketoglutarate dehydrogenase and possibly pyruvate dehydrogenase. Such a cascade of events is hypothesized, in this article, to occur in neurodegerative conditions such as Parkinson’s and Alzheimer’s disease.


Apart from this, though, inducible nitric oxide and superoxide anions are being produced via p38 MAPK in Alzheimer's disease, so there may be several routes by which the brain is being deprived of endothelial nitric oxide.


Lane Simonian
Posted: Tuesday, October 25, 2016 11:17 PM
Joined: 12/12/2011
Posts: 5158


I may have posted this one before, but it is a good one.

 2007 May;11(2):207-18.

Nitric oxide and nitroxidative stress in Alzheimer's disease.

Abstract

Nitric oxide is a signaling molecule produced by neurons and endothelial cells in the brain. NO is synthesized from L-arginine and oxygen by nitric oxide synthase: neuronal (nNOS), endothelial (eNOS), and inducible (iNOS). The endothelial NO acts as a vasorelaxant in the vasculature and as a neurotransmitter when produced by neurons (under the pathological conditions of Alzheimer's disease). NO can be scavenged in a rapid reaction with superoxide (O2-) to generate peroxynitrite (ONOO-), with a half-life of < 1 s. ONOO- is a potent oxidant and the primary component of nitroxidative stress. At high concentrations (> 100 nM), ONOO- can undergo homolytic or heterolytic cleavage to produce NO2+, NO2, and OH., highly reactive oxidative species and secondary components of nitroxidative stress. The high nitroxidative stress can initiate a cascade of redox reactions which can trigger apoptosis and evoke cytotoxic effects on neurons and endothelial cells. This article reviews the functions of NO and the potential role of NO/O2-/ONOO- induced nitroxidative stress in neuronal and endothelial degeneration observed in Alzheimer's disease.


Lane Simonian
Posted: Wednesday, October 26, 2016 10:52 AM
Joined: 12/12/2011
Posts: 5158


More on nitric oxide and peroxynitrite this time regarding the synthesis and release of acetylcholine--the main compound for the retrieval of short-term memory.

Both NO synthase inhibitors reduced the synthesis of ACh from the radioactive precursor acetate and its incorporation into synaptic vesicles as did ONOO- chemically synthesized or formed from SIN1. In addition, choline acetyltransferase activity was strongly inhibited by ONOO- and SIN1 but not by the NO donors SNAP and SNP or, by NO synthase inhibitors. Altogether these results indicate that NO and ONOO modulate presynaptic cholinergic metabolism in the micromolar range, NO (up to 100 microM) being a stimulating agent of ACh release and ONOO- being an inhibitor of ACh synthesis and choline acetyltransferase activity.




Lane Simonian
Posted: Wednesday, October 26, 2016 11:11 AM
Joined: 12/12/2011
Posts: 5158


A few more connections:

The Akt kinase signals directly to endothelial nitric oxide synthase

Two distinct signaling pathways regulate peroxynitrite-induced apoptosis in PC12 cells.

Peroxynitrite induces inactivation of the Akt pathway.


So not only is peroxynitrite reducing acetylcholine levels in the brain, it reduces the production of endothelial nitric oxide which is needed to increase acetylcholine levels in the brain.


conniestea
Posted: Thursday, October 27, 2016 5:19 PM
Joined: 10/27/2016
Posts: 1


Hi! I just started on this board and was reading about the different drug trials. Is it possible to get Peroxynitrite to give to a loved one to treat dementia?
Lane Simonian
Posted: Thursday, October 27, 2016 7:17 PM
Joined: 12/12/2011
Posts: 5158


Welcome, conniestea.  Several natural products contain compounds that scavenge peroxynitrite and may help in the treatment of Alzheimer's disease and to a certain degree other forms of dementia..  These include Korean red ginseng, heat processed ginseng (Korean red ginseng steamed at high temperatures), direct inhalation aromatherapy with various essential oils such as clove, bay laurel, lemon balm, and rosemary, and CBD oil high in cannabidiol and terpenes and low in THC.
Lane Simonian
Posted: Saturday, November 12, 2016 9:47 AM
Joined: 12/12/2011
Posts: 5158


A good abstract:

Author(s): Torreilles FSalmanTabcheh SGurin MTorreilles J


Abstract Inflammatory reaction is thought to be an important contributor to neuronal damage in neurodegenerative disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS) and the parkinsonism dementia complex of Guam. Among the toxic agents released in brain tissues by activated cells, we focus attention in this review on peroxynitrite, the product of the reaction between nitric oxide (NO) and superoxide. Peroxynitrite is a strong oxidizing and nitrating agent which can react with all classes of biomolecules. In the CNS it can be generated by microglial cells activated by pro-inflammatory cytokines or beta-amyloid peptide (beta-A) and by neurons in three different situations: hyperactivity of glutamate neurotransmission, mitochondrial dysfunction and depletion of L-arginine or tetrahydrobiopterin. The first two situations correspond to cellular responses to an initial neuronal injury and the peroxynitrite formed only exacerbates the inflammatory process, whereas in the third situation the peroxynitrite generated directly contributes to the initiation of the neurodegenerative process.


Lane Simonian
Posted: Thursday, December 1, 2016 11:14 AM
Joined: 12/12/2011
Posts: 5158


This recent study is quite interesting.

Peroxynitrite in the brain promotes the development of alzheimer's

Over the last twenty years, research studies have pointed to the accumulation of beta-amyloid protein aggregates (Abeta) as the main event at the origin of Alzheimer's. Now, a study led by Francisco José Muñoz, principal investigator at the Department of Experimental and Health Sciences of UPF, sheds light on the accumulation of these aggregates in the brain, discovering that the presence of peroxynitrite in the extracellular environment promotes the formation and stabilization of oligomeric beta-amyloid aggregates.

Beta-amyloid is a protein present in the nervous system whose function is not clear. Soluble beta-amyloid forms can aggregate giving rise to primary structures called oligomers, which in turn are added to give rise to mature fibers. According to some experts, the formation of mature fibers is a protective mechanism to avoid the presence of oligomers, since these have been described as the most toxic form of beta-amyloid. The oligomers directly alter the neuronal function and promote neurodegeneration.

Oligomers and beta-amyloid fibers induce nitro oxidative stress, triggering the production of nitric oxide and free radicals in the extracellular environment. When they combine, peroxynitrite is produced, a highly reactive molecule that can modify proteins and alter their function. The study led by Francisco José Muñoz reveals that when peroxynitrite reacts with beta-amyloid oligomers, it facilitates its stabilization and prevents the formation of mature fibers. Thus, the more beta-amyloid protein there is, the more peroxynitrite formation is promoted and the latter, in turn, makes the beta-amyloid oligomers to remain stabilized, perpetuating the characteristic neuronal damage of Alzheimer's disease.

Other studies suggest that amyloid fibers/plaques do not cause nitro-oxidative stress and that peroxynitrite-mediated nitration accelerates the conversion of oligomers into plaques. Still this study is an important contribution to our understanding of Alzheimer's disease.


Eden Desjardins
Posted: Friday, December 2, 2016 10:33 AM
Joined: 5/25/2015
Posts: 48


Thank you, Lane. Your in-depth analysis on these drugs are always appreciated. I've personally started my husband on tumeric a month ago and am seeing good results.
Lane Simonian
Posted: Friday, December 2, 2016 10:46 AM
Joined: 12/12/2011
Posts: 5158


Thank you, Eden.  I am happy to hear that tumeric is helping your husband. Positive reports always give me hope.
Lane Simonian
Posted: Saturday, December 3, 2016 9:45 AM
Joined: 12/12/2011
Posts: 5158


I am beginning to think the researchers in the study above reached the right conclusion: the peroxynitrite-mediated nitration of amyloid oligomers inhibits rather than accelerates their aggregation into plaques.  I remember another study which said that the peroxynitrite mediated nitration of tau inhibited its aggregation into tangles.  This would partially help explain why there are people who have relatively few plaques and tangles and yet have Alzheimer's disease and why there are other people with lots of plaques in their brains and some tangles who do not have Alzheimer's disease.  The key is not the aggregation of proteins it is the nitration and oxidation of proteins.  Various forms of amyloid (c-terminal fragments, amyloid oligomers, amyloid plaque in blood vessels) can contribute to this nitro-oxidative stress early on but so do many other factors.  This further explains why compounds that scavenge peroxynitrite and reverse part of the nitro-oxidative stress (such as eugenol in various essential oils; THC, cannabidiol, and terpenes such as eugenol in CBD oil,  and ferulic acid, syringic acid, vanillic acid, p-coumaric acid, and maltol) help partially reverse Alzheimer's disease whereas drugs that remove plaques and oligomers do not.
Lane Simonian
Posted: Tuesday, April 11, 2017 10:36 AM
Joined: 12/12/2011
Posts: 5158


The Role of Oxidative Damage in the Pathogenesis and Progression of Alzheimer's Disease and Vascular Dementia. 

Oxidative stress (OS) has been demonstrated to be involved in the pathogenesis of the two major types of dementia: Alzheimer's disease (AD) and vascular dementia (VaD). Evidence of OS and OS-related damage in AD is largely reported in the literature. Moreover, OS is not only linked to VaD, but also to all its risk factors.

This is also true for Alzheimer's disease: every risk factor for Alzheimer's disease increases oxidative stress.  This includes but is certainly not limited to amyloid beta.  That is why removing amyloid beta (likely even before the disease starts) puts only a small dent into the disease.

The cause of Alzheimer's disease is likely various oxidants and especially peroxynitrite. Specific antioxidants can likely be used to treat the disease.

Lane Simonian
Posted: Sunday, June 11, 2017 10:53 AM
Joined: 12/12/2011
Posts: 5158


I was inspired by a lead to look into the history of peroxynitrite and found some interesting information.  

"From 1901 until 1990, ca. 40 papers on peroxynitrite appeared. Since then, the number of publications has sharply increased to well over 12000 as a recent search (November 2014) on the Web of Science showed."


When the Good and the Bad Make the Ugly: The Discovery of Peroxynitrite

 

At first, no one took them seriously. In 1991, Rafael Radi, Joseph Beckman, Kenneth Bush, and Bruce Freeman published a paper in the Journal of Biological Chemistry (JBC) demonstrating that a molecule called peroxynitrite, the product of a reaction between nitric oxide and superoxide radicals, selectively attacked sulfhydryls in proteins. “Nobody believed much of any of it,” recalls Beckman at Oregon State University. “It was considered an unproven theory. I was surprised we even got the paper accepted in JBC.” ...

Radi says he and Beckman found inspiration from Clint Eastwood's movie “The Good, The Bad, and the Ugly.” It was unthinkable to physiologists that nitric oxide could “be converted in such a nasty molecule just because of the reaction with superoxide,” says Radi. “Nitric oxide was the good guy; superoxide, the bad; and peroxynitrite, the ugly.”...

These days, peroxynitrite is recognized as an oxidant and nucleophile that can attack mitochondria and lead to cell death by a slew of oxidation and nitration reactions. Radi explains that peroxynitrite has a dual personality. It can be “liberated by our immune cells to kill invading pathogens,” says Radi. However, he adds that the molecule has been implicated in atherosclerosis, hypertension, type 2 diabetes, and neurodegenerative conditions, such as amyotrophic lateral sclerosis...

However, back in the early 1990s, “it took a few years and redundant ways to show that these reactions were of any importance in biology,” says Radi. Beckman sees the silver lining in having naysayers: not too many others were interested in working on peroxynitrite. The field was left wide open for investigators like him, Radi, and Freeman to get a head start on peroxynitrite research. He says, “The moral here is don't get discouraged if people don't immediately jump to your ideas.”

http://www.jbc.org/content/290/52/30726.full

 


Lane Simonian
Posted: Sunday, June 25, 2017 10:47 AM
Joined: 12/12/2011
Posts: 5158


From a recent article:

"Abeta 1-42 raises peroxynitrite levels in astrocytes, and Abeta (1-42) toxicity can be inhibited by antioxidants, or by inhibition of nitric oxide (NO) formation (reactive oxygen species (ROS) and NO combine to form peroxynitrite), or by a scavenger of peroxynitrite."

Amyloid beta causes damage to astrocytes (which are critical for synaptic formation and subsequent neurotransmissions) and neurons by producing peroxynitrite.  Many other factors increase peroxynitrite formation including air pollutants, various pesticides, mercury exposure, chronic smoking, and a diet high in sugar, carbohydrates, and salt. This explains why efforts to remove amyloid have only slightly slowed down the progression of Alzheimer's disease.  It also explains why various substances containing peroxynitrite scavengers (marijuana, essential oils, and panax ginseng) have led to improvements in certain forms of memory and in some cases behavior.


Lane Simonian
Posted: Saturday, July 1, 2017 9:16 AM
Joined: 12/12/2011
Posts: 5158


From another recent article:

Peroxynitrite (ONOO) is a strong biological oxidant formed by the diffusion-limited reaction of nitric oxide (NO) and superoxide anion (O2radical dot). It has long been theorized that peroxynitrite generation could be the cause in a number of pathological conditions ranging from atherosclerosis to inflammatory, autoimmune, heart and neurodegenerative diseases. Its relatively long biological half-life and high reactivity allows peroxynitrite to oxidize a number of different targets in the cell. In physiologically relevant conditions peroxynitrite can directly react with thiols, or the radical products of peroxynitrite decomposition may indirectly oxidize other cellular components such as lipids, proteins and DNA. Downstream, oxidative modifications caused by peroxynitrite trigger cell death by a variety of mechanisms depending on the concentration of the oxidant. Peroxynitrite stimulates necrosis, apoptosis, autophagy, parthanatos and necroptosis. Here we review the mechanisms activated by peroxynitrite to cause neuronal death.

Compounds which inhibit the formation of and scavenge peroxynitrite have shown the greatest success in treating Alzheimer's disease.


Lane Simonian
Posted: Tuesday, December 19, 2017 10:15 PM
Joined: 12/12/2011
Posts: 5158


This is a really good article on the role of peroxynitrite in Alzheimer's disease.  First is a clear explanation of how peroxynitrite leads to the death of neurons.


Moreover, ONOO  [peroxynitrite] is suggested to cause protein aggregation still through nitrosylation of membrane protein thiols in mitochondria. This leads to the formation of pores which would compromise the structural and organizational integrity of the mitochondrial membrane, hence resulting in efflux of mitochondrial contents such as apoptosis inducing factors, consequently leading to apoptotic neuronal loss [51]. In addition, ATP production is severely compromised leading to inevitable cell death as reviewed elsewhere.


The authors then identify the critical problem in Alzheimer's disease:

Free radicals (ROS/RNS) are produced by normal metabolism and are involved in various physiological and pathological conditions. There is a homeostatic balance between free radical production and scavenging by antioxidants. Oxidative stress and nitrosative stress occur when this equilibrium is breached because the excessive ROS/RNS concentrations cannot be neutralized or countervailed by the existing antioxidant systems.

ROS: Radical oxygen species; RNS: Radical Nitrogen Species such as peroxynitrite.

And finally strategies for treating Alzheimer's disease:

The development of drugs aimed at downregulating oxidative stress and improving NO bioavailability in AD patients and other neurodegenerative diseases is a viable option and so is imperative. These approaches include antioxidants and anti-inflammatory mediators, calcium channel inhibitors/blockers and agents that could aid in Abeta clearance, and molecules which prevent and scavenge high concentrations of free radicals.

https://www.hindawi.com/journals/omcl/2016/7205747/


Lane Simonian
Posted: Sunday, June 10, 2018 10:19 AM
Joined: 12/12/2011
Posts: 5158


This one is for diabetes but with very critical implications for Alzheimer's disease:

Diabetes and hyperglycemia are associated with increased retinal oxidative and nitrative stress and vascular cell death. Paradoxically, high glucose stimulates expression of survival and angiogenic growth factors...HG [hyeprglycemia]- or PN [peroxynitritie]-treated cells also showed significant increases in tyrosine nitration on the p85 subunit of PI3-kinase [phosphatidylinositol 3-kinase] that inhibited its association with the catalytic p110 subunit and impaired PI3-kinase/Akt kinase activity. Decomposing peroxynitrite or blocking tyrosine nitration of p85 restored the activity of PI3-kinase, and prevented apoptosis and activation of p38 MAPK. Inhibiting p38 MAPK or overexpression of the constitutively activated Myr-Akt construct prevented HG- or peroxynitrite-mediated apoptosis. In conclusion, HG impairs pro-survival signals and causes accelerated EC [endothelial cells] apoptosis, at least in part via tyrosine nitration and inhibition of PI3-kinase. Inhibitors of nitration can be used in adjuvant therapy to delay diabetic retinopathy and microvascular complication. 

The exact same process occurs in Alzheimer's disease.  In the case of Alzheimer's disease the inhibition of the phosphatidylinositol 3-kinase leads to a decrease in blood flow and glucose transport in the brain (which can lead to delusions), an end to the regeneration of neurons and synapses in the hippocampus, and to the death of neurons (apoptosis).

When peroxynitrite is scavenged by various plants compounds (such as those found in CBD oil, essential oils via aromatherapy, and panax ginseng), it produces water and water is a de-nitrating agent.  When phosphatidylinositol 3-kinase activity is then partially restored through de-nitration, delusions decrease, neurons and synapses begin to be regenerated in the hippocampus (but unfortunately not in the cortex), and the death of neurons decreases. This is the reason why treatments with the above plant compounds have partially restored cognition in people with Alzheimer's disease. 


Lane Simonian
Posted: Saturday, August 4, 2018 10:36 AM
Joined: 12/12/2011
Posts: 5158


This from an article on tea compounds for the prevention and treatment of Alzheimer's disease.

EGCG may have preventive and/or therapeutic potential in AD patients by augmenting cellular antioxidant defense capacity and attenuating Abeta-mediated oxidative and/or nitrosative cell death. Abeta-induced damage of the neurons and glia are mediated via nitrosative and oxidative stress. BV2 cells exposed to Aβ underwent nitrosative stress, as shown by the increased expression of inducible nitric oxide synthase (iNOS) and subsequent production of nitric oxide (NO) and peroxynitrite, which were effectively suppressed by EGCG pretreatment. The mechanism considered to be at work is EGCG treatment fortifying the cellular GSH pool through elevated mRNA expression of gamma-glutamylcysteine ligase, a rate limiting enzyme in glutathione biosynthesis []. Tea polyphenols EGCG, EC, and TF suppressed oxidative stress-induced BACE-1 mRNA upregulation in neuronal cells, resulting in the reduction of amyloidogenic cleavage of APP and Abeta production [,]. Green tea extracts protected neuronal dPC12 cells from H2O2-induced and Abeta-induced cytotoxicity at concentration ranges of 0.3–10 μg/mL and 0.03–0.125 μg/mL, respectively [].


Amyloid beta is a product of nitro-oxidative stress and then it turns around and increases that stress.  The same is also true of certain herpes viruses and leukotrienes.  Remove amyloid (amyloid antibodies), use anti-virals medications against specific herpes viruses, and use asthma medications to prevent the development or block the effects of leukotrienes and you should be able to slow down the early progression of Alzheimer's disease.  But two problems with this approach, first there are many other sources of nitro-oxidative stress and secondly, the damage already done is not being reversed.

In contrast, certain plant compounds by scavenging hydrogen peroxide (H202) and peroxynitrite and by partially reversing oxidation and nitration lead to improvements in certain forms of memory in Alzheimer's disease that are sustained for two years.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659550/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5729264/




alexdged
Posted: Wednesday, May 15, 2019 11:12 PM
Joined: 5/15/2019
Posts: 1


Thank you, Lane, for this interesting article about Alzhimer's. I started to research on this area when my grandmother was diagnosed with Alzhimer's. But the prospects of getting healed seem to be slim, just like what it says in this page: Alzheimer's Therapies: A Reasonably Gloomy Update

https://blogs.sciencemag.org/pipeline/archives/2014/01/23/alzheimers_therapies_a_reasonably_gloomy_update

And, this page compiles all the inhibitors that could be used for Alzheimer's research.

https://www.bocsci.com/tag/alzheimer-s-disease-389.html

 


Lane Simonian
Posted: Thursday, May 16, 2019 2:49 PM
Joined: 12/12/2011
Posts: 5158


Thank you for posting, Alex.  I liked the list and summary of factors that are tied into Alzheimer's disease.