Blog Update

I’ve been writing a blog post every day for over three years. Most of those posts covered research in biology and medicine. I’m going to take a break from reading medical journal abstracts over the holidays. I’m planning on switching to a new format for my site that focuses on longer pages that discuss physiological systems or organs or classes of pharmaceuticals. I’ll probably focus on essays or other long form writing instead of trying to update a blog every day. Suggestions are welcome on what you would like me to write about. You can tweet me @snydr or email me at svsnyder@gmail.com

Giving Up Video Games

I think video games are works of art, but I’ve also given up other forms of art. Last year I stopped reading books. Just because you’re a male in the game playing demographic doesn’t mean you have to play games. This post outlines arguments in favor of giving up video games. Even more importantly, these reasons for not playing video games have nothing to do with any possible links between games and violence. Gaming takes time away from understanding and implementing scientific advancements in biology and medicine. Everyone’s life is worthless unless researchers succeed in curing aging.

Medicine:

• Playing games takes time away from important things like doing work on extending human lifespan.

• Playing games takes time away from reading medical journal articles and putting science-based medical findings into practice.

Physical:

• Sitting for long periods of time increases the mortality rate by promoting blood coagulation.

• Certain games are frightening and exacerbate the startle response and its negative effects on catecholamines.

Addiction:

• Games can be addictive yet have a low payoff.

• Games victimize people who are genetically susceptible to addiction and attention problems.

Financial:

• The cost of video games and consoles would be better spent on buying medication and access to therapy that helps people function better in life.

• New games and new consoles are too expensive in a world where unemployment and financial stress impact family finances.

• Subscriptions for online services create another financial drain for players.

• Digital game purchases have no resale value.

• Many playthroughs are available on YouTube where you can watch someone else play instead of having to buy a game.

• Some games require expensive controllers or other peripherals.

Game Companies:

• Game companies have overpaid executives.

• Game publishers exploit development companies who have less bargaining power.

• Unpaid overtime is abused in game development production cycles.

• Games can be canceled or become vaporware because of mistakes in planning and management.

• The game industry is trying to use anticompetitive practices to eliminate the used game market.

• Game retailers use upselling techniques and membership programs that annoy customers.

• The time programmers spend on creating games would be better spent on bioinformatics or health applications.

• Game developers have lower revenue, profit, and valuations than companies in other industries and therefore have fewer financial opportunities.

• The game industry is hit-driven, which leads to precarious employment for programmers.

Gamers:

• Many gamers focus on trivial things instead of important things like extending human lifespan.

• Gamers have low status in society. Being a skilled gamer is much lower status than being a doctor or CEO or director of a research lab.

• Many gamers are arrogant and think their opinons matter when they are really just animals without free will whose lives are worthless since they die like other human beings.

• Some girl gamers are attention seekers and some male gamers are too.

• Many online gamers are children, and few of them have any useful knowledge to offer on important non-game topics.

• There are rude and offensive players in multiplayer games.

Technical:

• Many games lack effective quality assurance which is reflected in glitches.

• Graphics advances are not as noticeable as they could be between the most recent generations of consoles.

• Loading times are frustrating.

• Certain consoles have a lack of backwards compatibility.

• Lag can be frustrating in online games.

• Some games lack online play.

• Control schemes are difficult to design to reach the sweet spot between too easy and too difficult.

• Superior artificial intelligence rarely exists in games.

• Soundtracks can lack rich soundscapes.

• Frame rate abnormalities can occur in games.

Reviews:

• The vast majority of games receive average or poor reviews because of their copycat nature and lack of fun.

• The reliance on advertising revenue skews reviews coming from game media companies.

Social:

• Games promote false ideas about how the world really works.

• Many games promote unrealistic images of both women and men and their bodies.

• Game fandom is still less socially acceptable than other hobbies such as sports fandom or movie fandom.

Environmental:

• The manufacturing process for making video game consoles involves toxic chemicals.

• Running video game consoles requires electricity and power generation, which has negative environmental effects on the planet.

Gameplay:

• Many games involve tedious tasks like hunting for an object or retracing steps.

• It’s tedious to upgrade characters.

• Games can have short campaigns.

• Games can lack replay value.

• Many games can be too linear for some people.

• Difficulty is either too hard or too easy.

• Difficulty doesn’t change automatically based on skill.

• Mobile games rehash or copy old obsolete games.

• Stealth gameplay can be annoying.

• Writing a good story takes too much effort for some game designers.

• On rails shooter segments can lack creativity.

• Voice acting is bad in many games.

• Platforming segments can be frustrating.

• Puzzles can be frustrating.

• Bad camera angles can ruin gameplay.

• Level design can be uninspired.

• Tutorials can be unhelpful or require memorization for too many things.

• Humor is difficult to get right in games.

• Games have to walk a difficult line between insufficient character customization or overwhelming character customization.

• Boss fights can be too difficult or too easy and unsatisfying.

Longevity and Perfection

As long as people continue to die, it doesn’t matter whether they die at age one or at age one hundred. It’s a tragedy when a baby dies in infancy, but it would also be a tragedy if they died in old age. Death means that all the time people invest in themselves and their families is ultimately pointless. Even if a person is remembered in a positive way, it doesn’t matter to the person who dies, since that individual will still be dead. Life is pointless and meaningless as long as everyone dies in the end anyway.

Thinking death is good or even acceptable simply because it’s natural is the naturalistic fallacy in action. Rape is natural, but it’s still bad and people are working to end sexual violence. Aging and death are the same way. I have anxiety disorders and live in fear of death, so those who think anti-aging research is unnecessary are ableist against people afflicted with anxiety. Another reason people accept death is due to their religious beliefs. Even if people are religious, they still need to be concerned that they could be following the wrong religion and running the risk of ending up in hell as a result. Therefore it’s good to pursue life extension as a backup plan.

Life needs to involve an obsession with perfectly predicting the future, which is very difficult and maybe even impossible. Why is it so important to predict the future? America lacks sufficient social safety nets and has a culture of judgment and blame. This means people have to be able to predict the future with perfect accuracy. Even though the lives of people are controlled by corporations and governments and powerful individuals, the average person is still expected to take “personal responsibility” for everything single thing that happens to him or her. If you make a big mistake, people will say that it’s entirely your fault and that you deserve to suffer. The widespread belief in the myth of free will and the religion of personal responsibility leads many Americans to think the individual is entirely responsible for any negative outcome that happens to him or her. Just look at most comments on the web where people make the mistake of trying to ask for help. Some Americans combine the worst of both worlds, holding opinions that are both cruel and illogical. People seem to think that if a person gets sick, experiences financial difficulties, gets the wrong degree, has emotional problems, marries the wrong person, etc – it’s entirely that individual’s fault and they deserve to suffer alone.

Even worse, those types of people seem to have power to decide which people can get jobs and healthcare. A possible outcome might go like this: get sick -> can’t work -> lose job -> lose health insurance -> can’t get healthcare -> can’t get another job -> go bankrupt -> get sicker -> die. I take around forty supplement pills a day, not only because I live in fear of death every day since no one knows for sure what happens after death, but also because sickness can lead to a ruined life via the pathway outlined above. I feel guilty whenever I have fun instead of spending time reading medical journals and finding biomedical studies with predictive power.

There are also violent people with animal urges who still roam free. People with a biological propensity towards violence can’t be arrested until they actually commit a crime, so the only thing to do is hope you aren’t the first victim when their psychopathy manifests itself. Until everyone’s brains are scanned to identify neurological correlates of violent behavior, there are plenty of violent people who are ticking time bombs just walking around. It’s not just a gun control problem. These violent people can find lots of inventive ways to kill someone, especially if they rise to positions of power.

Life extension can give meaning to human life. If life expectancy can be extended indefinitely, life will finally mean something because a person can continue to exist. Changing brain chemistry to generate feelings of meaning in life is another potential solution.

Amygdala Drug Effects

The following medications and compounds reduce activity in the human amygdala. This indicates they are useful in treating anxiety disorders.

Alcohol

Cannabidiol

D-cycloserine

Diazepam

Escitalopram

Lorazepam

Paroxetine

Pregabalin

Propranolol

References:

Altered affective response in marijuana smokers: an FMRI study. http://www.ncbi.nlm.nih.gov/pubmed/19656642

Amygdala volume reductions in pediatric patients with obsessive-compulsive disorder treated with paroxetine: preliminary findings. http://www.ncbi.nlm.nih.gov/pubmed/14970831

D-cycloserine inhibits amygdala responses during repeated presentations of faces. http://www.ncbi.nlm.nih.gov/pubmed/17667888

Distinct effects of {delta}9-tetrahydrocannabinol and cannabidiol on neural activation during emotional processing. http://www.ncbi.nlm.nih.gov/pubmed/19124693

Dose-dependent decrease of activation in bilateral amygdala and insula by lorazepam during emotion processing. http://www.ncbi.nlm.nih.gov/pubmed/15753241

Effects of alcohol on brain responses to social signals of threat in humans. http://www.ncbi.nlm.nih.gov/pubmed/21122818

Effects of diazepam on BOLD activation during the processing of aversive faces. http://www.ncbi.nlm.nih.gov/pubmed/21106607

Escitalopram effects on insula and amygdala BOLD activation during emotional processing. http://www.ncbi.nlm.nih.gov/pubmed/18058090

Human amygdala reactivity is diminished by the β-noradrenergic antagonist propranolol. http://www.ncbi.nlm.nih.gov/pubmed/20102667

Modulation of effective connectivity during emotional processing by Delta 9-tetrahydrocannabinol and cannabidiol. http://www.ncbi.nlm.nih.gov/pubmed/19775500

Pregabalin influences insula and amygdala activation during anticipation of emotional images. http://www.ncbi.nlm.nih.gov/pubmed/21430645

Nutrigenomics

Studies from the field of nutrigenomics show that the following foods lead to beneficial genetic changes

Chlorella

Cocoa

Green Tea

Mediterranean Diet

Olive Oil

Omega-3 Fatty Acids

Orange Juice

Tomato Extract

Vegetables

References:

An antiinflammatory dietary mix modulates inflammation and oxidative and metabolic stress in overweight men: a nutrigenomics approach. http://www.ncbi.nlm.nih.gov/pubmed/20181810

Characterization of human gene expression changes after olive oil ingestion: an exploratory approach. http://www.ncbi.nlm.nih.gov/pubmed/19545487

Effects of cocoa extract and dark chocolate on angiotensin-converting enzyme and nitric oxide in human endothelial cells and healthy volunteers–a nutrigenomics perspective. http://www.ncbi.nlm.nih.gov/pubmed/20966764

Hesperidin displays relevant role in the nutrigenomic effect of orange juice on blood leukocytes in human volunteers: a randomized controlled cross-over study. http://www.ncbi.nlm.nih.gov/pubmed/22110589

In vivo nutrigenomic effects of virgin olive oil polyphenols within the frame of the Mediterranean diet: a randomized controlled trial. http://www.ncbi.nlm.nih.gov/pubmed/20179144

In vivo transcriptomic profile after a Mediterranean diet in high-cardiovascular risk patients: a randomized controlled trial. http://www.ncbi.nlm.nih.gov/pubmed/23902780

Mononuclear cell transcriptome response after sustained virgin olive oil consumption in humans: an exploratory nutrigenomics study. http://www.ncbi.nlm.nih.gov/pubmed/19290808

Nutrigenomic studies of effects of Chlorella on subjects with high-risk factors for lifestyle-related disease. http://www.ncbi.nlm.nih.gov/pubmed/18800884

Nutrigenomics approach elucidates health-promoting effects of high vegetable intake in lean and obese men. http://www.ncbi.nlm.nih.gov/pubmed/23595524

Time course of changes in the expression of insulin sensitivity-related genes after an acute load of virgin olive oil. http://www.ncbi.nlm.nih.gov/pubmed/19422291

Skin Rejuvenation

These nutraceuticals have proven successful in rejuvenating skin in lab animal experiments:

alpha-tocopherol

coenzyme Q10

green tea

L-methionine

salidroside

soy phospholipids

References:

Beneficial effects of pro-/antioxidant-based nutraceuticals in the skin rejuvenation techniques. http://www.ncbi.nlm.nih.gov/pubmed/17519117

Green tea and red light–a powerful duo in skin rejuvenation. http://www.ncbi.nlm.nih.gov/pubmed/19817517

Rejuvenating activity of salidroside (SDS): dietary intake of SDS enhances the immune response of aged rats. http://www.ncbi.nlm.nih.gov/pubmed/22367581

Food and Hair

These foods and compounds increase hair growth or improve hair in lab animals:

apple procyanidin

choline-stabilized orthosilicic acid

dietary isoflavones

polyunsaturated fatty acids

References:

Dietary isoflavone increases insulin-like growth factor-I production, thereby promoting hair growth in mice. http://www.ncbi.nlm.nih.gov/pubmed/20576422

Effect of oral intake of choline-stabilized orthosilicic acid on hair tensile strength and morphology in women with fine hair. http://www.ncbi.nlm.nih.gov/pubmed/17960402

Investigation of topical application of procyanidin B-2 from apple to identify its potential use as a hair growing agent. http://www.ncbi.nlm.nih.gov/pubmed/11194183

Skin surface lipids and skin and hair coat condition in dogs fed increased total fat diets containing polyunsaturated fatty acids. http://www.ncbi.nlm.nih.gov/pubmed/18700855

Amyotrophic Lateral Sclerosis Treatments

Animal experiments indicate there are some promising potential treatments for amyotrophic lateral sclerosis. While there’s no true cure for ALS yet, some of these experiments show that new compounds and natural substances can treat symptoms and extend lifespan.

They include:

3-4 diaminopyridine

5-Hydroxytryptophan

5D10

Acetyl-L-Carnitine

Activated Protein C

AEOL 10150

AGS-499

AM-1241

Ammonium tetrathiomolybdate

Angiogenin

Arimoclomol

Ascorbate

Bee Venom

Caffeic Acid Phenethyl Ester

Cannabinol

Caprylic Triglyceride

Celastrol

CK-2017357

Clenbuterol

Colivelin

Creatine

Cyclosporine

D-Penicillamine

Dasatinib

Davunetide

Delta(9)-tetrahydrocannabinol

Dexpramipexole

Diallyl Trisulfide

Dichloroacetate

Dihydrotestosterone

Dimebon

DL-3-n-butylphthalide

DP-109

DP-460

Edaravone

EGb761 (Gingko Biloba Extract)

ENKAD

Epigallocatechin-3-gallate (EGCG)

Exendin-4

Fasudil

Folic Acid

Galactooligosaccharide

Gemals

Ginseng Root

GPI-1046

Granulocyte Colony Stimulating Factor

GSK-3 inhibitor VIII

Heat Shock Protein 70

Hepatocyte Growth Factor

HLA20

Iron Porphyrin

Ivermectin

Jiawei Sijunzi (JWSJZ)

L-745,870

L-arginine

Lead

Lenalidomide

Lipoic Acid

M30

Manganese Porphyrin

Melatonin

Memantine

Methionine Sulfoximine

Milk Whey Proteins

N-acetyl-L-cysteine

Nortriptyline

Olesoxime

Oxidized Galectin-1

P7C3A20

Pegfilgrastim

Phenylbutyrate

Pioglitazone

Polyamine-Modified Catalase

PRE-084

Progesterone

Pyruvate

Rasagiline

Recombinant Human Erythropoietin

Recombinant Human Insulinlike Growth Factor-I (rhIGF-I)

Resveratrol

Riluzole

Ro 28-2653

RPR 119990

S-adenosyl Methionine

S[+]-Apomorphine

Scolopendra Subspinipes Mutilans

Semapimod

SK-PC-B70M

Sodium Phenylbutyrate

Suppressor Factor

Talampanel

TAT-modified Bcl-X(L)

Tempol

Tianeptine

Trichostatin A

Trientine

TRO19622

Uridine

Vascular Endothelial Growth Factor

Vincristine

Vitamin D3

Vitamin E

VK-28

Wen-Pi-Tang

ZK 187638

References:

A dopamine receptor antagonist L-745,870 suppresses microglia activation in spinal cord and mitigates the progression in ALS model mice. http://www.ncbi.nlm.nih.gov/pubmed/18423451

A double-blind study of the effectiveness of cyclosporine in amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/3281637

A phase II trial of talampanel in subjects with amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19961264

A pilot trial of memantine and riluzole in ALS: correlation to CSF biomarkers. http://www.ncbi.nlm.nih.gov/pubmed/20839903

Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells. http://www.ncbi.nlm.nih.gov/pubmed/19841542

Additive neuroprotective effects of a histone deacetylase inhibitor and a catalytic antioxidant in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16289867

AM1241, a cannabinoid CB2 receptor selective compound, delays disease progression in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16781706

Ammonium tetrathiomolybdate delays onset, prolongs survival, and slows progression of disease in a mouse model for amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18617166

Amyotrophic lateral sclerosis: delayed disease progression in mice by treatment with a cannabinoid. http://www.ncbi.nlm.nih.gov/pubmed/15204022

An ALS mouse model with a permeable blood-brain barrier benefits from systemic cyclosporine A treatment. http://www.ncbi.nlm.nih.gov/pubmed/14756802

An attempt to inhibit the course of amyotrophic lateral sclerosis (ALS) by suppressor factor. http://www.ncbi.nlm.nih.gov/pubmed/8993772

Autophagy activation and neuroprotection by progesterone in the G93A-SOD1 transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23891729

Bee venom attenuates neuroinflammatory events and extends survival in amyotrophic lateral sclerosis models. http://www.ncbi.nlm.nih.gov/pubmed/20950451

Beneficial effect of ginseng root in SOD-1 (G93A) transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/11090864

Benefit of a combined treatment with trientine and ascorbate in familial amyotrophic lateral sclerosis model mice. http://www.ncbi.nlm.nih.gov/pubmed/10327155

Benefit of tianeptine and morphine in a transgenic model of familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16546757

c-Abl inhibition delays motor neuron degeneration in the G93A mouse, an animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23049975

Caffeic acid phenethyl ester extends survival of a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22206942

Cannabinol delays symptom onset in SOD1 (G93A) transgenic mice without affecting survival. http://www.ncbi.nlm.nih.gov/pubmed/16183560

Caprylic triglyceride as a novel therapeutic approach to effectively improve the performance and attenuate the symptoms due to the motor neuron loss in ALS disease. http://www.ncbi.nlm.nih.gov/pubmed/23145119

Celastrol blocks neuronal cell death and extends life in transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16909005

Chemotherapy delays progression of motor neuron disease in the SOD1 G93A transgenic mouse. http://www.ncbi.nlm.nih.gov/pubmed/15282441

Colivelin prolongs survival of an ALS model mouse. http://www.ncbi.nlm.nih.gov/pubmed/16564029

Combined riluzole and sodium phenylbutyrate therapy in transgenic amyotrophic lateral sclerosis mice. http://www.ncbi.nlm.nih.gov/pubmed/18618304

Control of motoneuron survival by angiogenin. http://www.ncbi.nlm.nih.gov/pubmed/19109488

Death receptor 6 (DR6) antagonist antibody is neuroprotective in the mouse SOD1(G93A) model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/24113175

Dexpramipexole effects on functional decline and survival in subjects with amyotrophic lateral sclerosis in a Phase II study: subgroup analysis of demographic and clinical characteristics. http://www.ncbi.nlm.nih.gov/pubmed/22985432

Dietary supplementation with S-adenosyl methionine delays the onset of motor neuron pathology in a murine model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19757209

Dietary vitamin D3 supplementation at 10× the adequate intake improves functional capacity in the G93A transgenic mouse model of ALS, a pilot study. http://www.ncbi.nlm.nih.gov/pubmed/22591278

Dihydrotestosterone ameliorates degeneration in muscle, axons and motoneurons and improves motor function in amyotrophic lateral sclerosis model mice. http://www.ncbi.nlm.nih.gov/pubmed/22606355

Dimebon slows progression of proteinopathy in γ-synuclein transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/22179976

DL-3-n-butylphthalide extends survival by attenuating glial activation in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22056419

Effect of nutritional supplementation with milk whey proteins in amyotrophic lateral sclerosis patients. http://www.ncbi.nlm.nih.gov/pubmed/20464297

Effect of recombinant human insulin-like growth factor-I on progression of ALS. A placebo-controlled study. The North America ALS/IGF-I Study Group. http://www.ncbi.nlm.nih.gov/pubmed/9409357

Effect of sex on lifespan, disease progression, and the response to methionine sulfoximine in the SOD1 G93A mouse model for ALS. http://www.ncbi.nlm.nih.gov/pubmed/23217569

Effects of 3-4 diaminopyridine (DAP) in motor neuron diseases. http://www.ncbi.nlm.nih.gov/pubmed/21321491

Effects of an inhibitor of poly(ADP-ribose) polymerase, desmethylselegiline, trientine, and lipoic acid in transgenic ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/11259130

Exendin-4 ameliorates motor neuron degeneration in cellular and animal models of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22384126

Exogenous delivery of heat shock protein 70 increases lifespan in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18045911

Fasudil, a rho kinase inhibitor, limits motor neuron loss in experimental models of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23763343

Folic acid protects motor neurons against the increased homocysteine, inflammation and apoptosis in SOD1 G93A transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/18436268

Galactooligosaccharide improves the animal survival and alleviates motor neuron death in SOD1G93A mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23673277

Gemals, a new drug candidate, extends lifespan and improves electromyographic parameters in a rat model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18428000

Glutamate AMPA receptors change in motor neurons of SOD1G93A transgenic mice and their inhibition by a noncompetitive antagonist ameliorates the progression of amytrophic lateral sclerosis-like disease. http://www.ncbi.nlm.nih.gov/pubmed/16323214

Granulocyte colony stimulating factor attenuates inflammation in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21711557

Granulocyte-colony stimulating factor improves outcome in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18835867

Identification and characterization of cholest-4-en-3-one, oxime (TRO19622), a novel drug candidate for amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17496168

Inhibition of glycogen synthase kinase-3 suppresses the onset of symptoms and disease progression of G93A-SOD1 mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/17433298

Inhibition of p38 mitogen activated protein kinase activation and mutant SOD1(G93A)-induced motor neuron death. http://www.ncbi.nlm.nih.gov/pubmed/17346981

Intake of polyunsaturated fatty acids and vitamin E reduces the risk of developing amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16648143

Intracerebroventricular infusion of monoclonal antibody or its derived Fab fragment against misfolded forms of SOD1 mutant delays mortality in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/20345765

Intrathecal cyclosporin prolongs survival of late-stage ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/11251210

Intrathecal delivery of hepatocyte growth factor from amyotrophic lateral sclerosis onset suppresses disease progression in rat amyotrophic lateral sclerosis model. http://www.ncbi.nlm.nih.gov/pubmed/17984685

Investigation of the therapeutic effects of edaravone, a free radical scavenger, on amyotrophic lateral sclerosis (Phase II study). http://www.ncbi.nlm.nih.gov/pubmed/17127563

Iron porphyrin treatment extends survival in a transgenic animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/12641736

Ivermectin inhibits AMPA receptor-mediated excitotoxicity in cultured motor neurons and extends the life span of a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17045808

Late stage treatment with arimoclomol delays disease progression and prevents protein aggregation in the SOD1 mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/18673445

Lead exposure stimulates VEGF expression in the spinal cord and extends survival in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/19914377

Lenalidomide (Revlimid) administration at symptom onset is neuroprotective in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19733563

Life span extension and reduced neuronal death after weekly intraventricular cyclosporin injections in the G93A transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15255263

Manganese porphyrin given at symptom onset markedly extends survival of ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/16049935

Mechano-growth factor, an IGF-I splice variant, rescues motoneurons and improves muscle function in SOD1(G93A) mice. http://www.ncbi.nlm.nih.gov/pubmed/19038252

Melatonin inhibits the caspase-1/cytochrome c/caspase-3 cell death pathway, inhibits MT1 receptor loss and delays disease progression in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23537713

Memantine prolongs survival in an amyotrophic lateral sclerosis mouse model. http://www.ncbi.nlm.nih.gov/pubmed/16262676

Methionine sulfoximine, an inhibitor of glutamine synthetase, lowers brain glutamine and glutamate in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/20060132

Modulation of astrocytic mitochondrial function by dichloroacetate improves survival and motor performance in inherited amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22509356

Motor neuronal protection by L-arginine prolongs survival of mutant SOD1 (G93A) ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/19427829

MRS study of the effects of minocycline on markers of neuronal and microglial integrity in ALS. http://www.ncbi.nlm.nih.gov/pubmed/20832222

Muscle-derived but not centrally derived transgene GDNF is neuroprotective in G93A-SOD1 mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/17034790

N-acetyl-L-cysteine improves survival and preserves motor performance in an animal model of familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/10943709

NAP (davunetide) modifies disease progression in a mouse model of severe neurodegeneration: protection against impairments in axonal transport. http://www.ncbi.nlm.nih.gov/pubmed/23631872

Neurochemical correlates of differential neuroprotection by long-term dietary creatine supplementation. http://www.ncbi.nlm.nih.gov/pubmed/16140286

Neuroprotective and neuritogenic activities of novel multimodal iron-chelating drugs in motor-neuron-like NSC-34 cells and transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19638399

Neuroprotective effect of oxidized galectin-1 in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15899257

Neuroprotective effects of (-)-epigallocatechin-3-gallate in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17021948

Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/10086395

Neuroprotective effects of diallyl trisulfide in SOD1-G93A transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21147075

Neuroprotective effects of the Sigma-1 receptor (S1R) agonist PRE-084, in a mouse model of motor neuron disease not linked to SOD1 mutation. http://www.ncbi.nlm.nih.gov/pubmed/24141020

Neuroprotective efficacy of aminopropyl carbazoles in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23027932

Nortriptyline delays disease onset in models of chronic neurodegeneration. http://www.ncbi.nlm.nih.gov/pubmed/17686041

Novel telomerase-increasing compound in mouse brain delays the onset of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22351600

Olesoxime delays muscle denervation, astrogliosis, microglial activation and motoneuron death in an ALS mouse model. http://www.ncbi.nlm.nih.gov/pubmed/22369784

Open Randomized Clinical Trial on JWSJZ Decoction for the Treatment of ALS Patients. http://www.ncbi.nlm.nih.gov/pubmed/24093046

Peroxisome proliferator-activated receptor-gamma agonist extends survival in transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15649489

Preliminary investigation of effect of granulocyte colony stimulating factor on amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19922135

Prevention of motor neuron degeneration by novel iron chelators in SOD1(G93A) transgenic mice of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21346313

Pyruvate slows disease progression in a G93A SOD1 mutant transgenic mouse model. http://www.ncbi.nlm.nih.gov/pubmed/17174029

Randomized double-blind placebo-controlled trial of acetyl-L-carnitine for ALS. http://www.ncbi.nlm.nih.gov/pubmed/23421600

Rasagiline alone and in combination with riluzole prolongs survival in an ALS mouse model. http://www.ncbi.nlm.nih.gov/pubmed/15372249

Recombinant human erythropoietin suppresses symptom onset and progression of G93A-SOD1 mouse model of ALS by preventing motor neuron death and inflammation. http://www.ncbi.nlm.nih.gov/pubmed/17439481

Reduced oxidative damage in ALS by high-dose enteral melatonin treatment. http://www.ncbi.nlm.nih.gov/pubmed/17014688

Regenerative therapies for amyotrophic lateral sclerosis using hepatocyte growth factor. http://www.ncbi.nlm.nih.gov/pubmed/22277532

Resveratrol upregulated heat shock proteins and extended the survival of G93A-SOD1 mice. http://www.ncbi.nlm.nih.gov/pubmed/23000195

RPR 119990, a novel alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid antagonist: synthesis, pharmacological properties, and activity in an animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/11561094

S[+] Apomorphine is a CNS penetrating activator of the Nrf2-ARE pathway with activity in mouse and patient fibroblast models of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23608463

Safety, tolerability and pharmacodynamics of a skeletal muscle activator in amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22591195

Scolopendra subspinipes mutilans attenuates neuroinflammation in symptomatic hSOD1G93A mice. http://www.ncbi.nlm.nih.gov/pubmed/24168240

Selective up-regulation of the glial Na+-dependent glutamate transporter GLT1 by a neuroimmunophilin ligand results in neuroprotection. http://www.ncbi.nlm.nih.gov/pubmed/16274998

Sigma-1R agonist improves motor function and motoneuron survival in ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/22935988

SK-PC-B70M alleviates neurologic symptoms in G93A-SOD1 amyotrophic lateral sclerosis mice. http://www.ncbi.nlm.nih.gov/pubmed/20971081

Tempol moderately extends survival in a hSOD1(G93A) ALS rat model by inhibiting neuronal cell loss, oxidative damage and levels of non-native hSOD1(G93A) forms. http://www.ncbi.nlm.nih.gov/pubmed/23405225

The CB2 cannabinoid agonist AM-1241 prolongs survival in a transgenic mouse model of amyotrophic lateral sclerosis when initiated at symptom onset. http://www.ncbi.nlm.nih.gov/pubmed/17241118

The Chinese prescription Wen-Pi-Tang extract delays disease onset in amyotrophic lateral sclerosis model mice while attenuating the activation of glial cells in the spinal cord. http://www.ncbi.nlm.nih.gov/pubmed/19252282

The copper chelator d-penicillamine delays onset of disease and extends survival in a transgenic mouse model of familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/9240414

The effect of epigallocatechin gallate on suppressing disease progression of ALS model mice. http://www.ncbi.nlm.nih.gov/pubmed/16356650

The lipophilic metal chelators DP-109 and DP-460 are neuroprotective in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17630988

The matrix metalloproteinases inhibitor Ro 28-2653 [correction of Ro 26-2853] extends survival in transgenic ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/16516196

The oral antidiabetic pioglitazone protects from neurodegeneration and amyotrophic lateral sclerosis-like symptoms in superoxide dismutase-G93A transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/16120782

The serotonin precursor 5-hydroxytryptophan delays neuromuscular disease in murine familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/14527871

Therapeutic benefit of polyamine-modified catalase as a scavenger of hydrogen peroxide and nitric oxide in familial amyotrophic lateral sclerosis transgenics. http://www.ncbi.nlm.nih.gov/pubmed/11117554

Therapeutic benefits of intrathecal protein therapy in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18543336

Therapeutic effects of clenbuterol in a murine model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16388902

Therapeutic effects of dl-3-n-butylphthalide in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22800896

Therapeutic efficacy of EGb761 (Gingko biloba extract) in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/11665866

Treatment of amyotrophic lateral sclerosis with ribonucleotides. http://www.ncbi.nlm.nih.gov/pubmed/1266475

Treatment with arimoclomol, a coinducer of heat shock proteins, delays disease progression in ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/15034571

Treatment with edaravone, initiated at symptom onset, slows motor decline and decreases SOD1 deposition in ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/18718468

Treatment with trichostatin A initiated after disease onset delays disease progression and increases survival in a mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21712032

Uridine ameliorates the pathological phenotype in transgenic G93A-ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/20565334

Vascular endothelial growth factor prolongs survival in a transgenic mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/15389897

VEGF delivery with retrogradely transported lentivector prolongs survival in a mouse ALS model. http://www.ncbi.nlm.nih.gov/pubmed/15164063

Vitamin D deficiency and its supplementation in patients with amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23815870

Vitamin E intake and risk of amyotrophic lateral sclerosis: a pooled analysis of data from 5 prospective cohort studies. http://www.ncbi.nlm.nih.gov/pubmed/21335424

Vitamin E intake and risk of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15529299

Vitamin E serum levels and controlled supplementation and risk of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23286756

Amyotrophic Lateral Sclerosis Gene Therapy

Experiments in lab animals indicate gene therapy could extend lifespan in amyotrophic lateral sclerosis.

References:

AAV4-mediated expression of IGF-1 and VEGF within cellular components of the ventricular system improves survival outcome in familial ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/20859261

CNS-targeted viral delivery of G-CSF in an animal model for ALS: improved efficacy and preservation of the neuromuscular unit. http://www.ncbi.nlm.nih.gov/pubmed/21139572

Gene therapy of murine motor neuron disease using adenoviral vectors for neurotrophic factors. http://www.ncbi.nlm.nih.gov/pubmed/9095177

Increased survival and function of SOD1 mice after glial cell-derived neurotrophic factor gene therapy. http://www.ncbi.nlm.nih.gov/pubmed/12067438

Intraparenchymal spinal cord delivery of adeno-associated virus IGF-1 is protective in the SOD1G93A model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/17963733

Intraspinal cord delivery of IGF-I mediated by adeno-associated virus 2 is neuroprotective in a rat model of familial ALS. http://www.ncbi.nlm.nih.gov/pubmed/19135533

Nerve injection of viral vectors efficiently transfers transgenes into motor neurons and delivers RNAi therapy against ALS. http://www.ncbi.nlm.nih.gov/pubmed/19344276

Neuroprotective effects of glial cell line-derived neurotrophic factor mediated by an adeno-associated virus vector in a transgenic animal model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/12177190

Rescue of amyotrophic lateral sclerosis phenotype in a mouse model by intravenous AAV9-ADAR2 delivery to motor neurons. http://www.ncbi.nlm.nih.gov/pubmed/24115583

Retrograde viral delivery of IGF-1 prolongs survival in a mouse ALS model. http://www.ncbi.nlm.nih.gov/pubmed/12907804

Therapeutic AAV9-mediated Suppression of Mutant SOD1 Slows Disease Progression and Extends Survival in Models of Inherited ALS. http://www.ncbi.nlm.nih.gov/pubmed/24008656

Viral delivery of antioxidant genes as a therapeutic strategy in experimental models of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/23732987

Virus-delivered small RNA silencing sustains strength in amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/15852369

Widespread spinal cord transduction by intrathecal injection of rAAV delivers efficacious RNAi therapy for amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/24108104

Cell Therapy ALS Treatments

Cell transplants, including stem cell transplants, have shown some success in treating amyotrophic lateral sclerosis symptoms in lab animal experiments. There are even a few human experiments that have slowed the progression of the disease somewhat.

References:

A novel cell transplantation protocol and its application to an ALS mouse model. http://www.ncbi.nlm.nih.gov/pubmed/18691571

Autologous mesenchymal stem cells: clinical applications in amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/16808883

Bone marrow stem cell transplantation in amyotrophic lateral sclerosis: technical aspects and preliminary results from a clinical trial. http://www.ncbi.nlm.nih.gov/pubmed/21381286

Chimerization of astroglial population in the lumbar spinal cord after mesenchymal stem cell transplantation prolongs survival in a rat model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19267424

Combined immunosuppressive agents or CD4 antibodies prolong survival of human neural stem cell grafts and improve disease outcomes in amyotrophic lateral sclerosis transgenic mice. http://www.ncbi.nlm.nih.gov/pubmed/16644922

Direct muscle delivery of GDNF with human mesenchymal stem cells improves motor neuron survival and function in a rat model of familial ALS. http://www.ncbi.nlm.nih.gov/pubmed/18797452

Dose-dependent efficacy of ALS-human mesenchymal stem cells transplantation into cisterna magna in SOD1-G93A ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/19879334

Feasibility, safety, and preliminary proof of principles of autologous neural stem cell treatment combined with T-cell vaccination for ALS patients. http://www.ncbi.nlm.nih.gov/pubmed/22507681

Fetal olfactory ensheathing cells transplantation in amyotrophic lateral sclerosis patients: a controlled pilot study. http://www.ncbi.nlm.nih.gov/pubmed/18673377

Human mesenchymal stem cell transplantation extends survival, improves motor performance and decreases neuroinflammation in mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/18586098

Human mesenchymal stromal cells ameliorate the phenotype of SOD1-G93A ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/17786603

Human umbilical cord blood treatment in a mouse model of ALS: optimization of cell dose. http://www.ncbi.nlm.nih.gov/pubmed/18575617

Intra-bone marrow-bone marrow transplantation slows disease progression and prolongs survival in G93A mutant SOD1 transgenic mice, an animal model mouse for amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19686706

Intracerebroventricular injection of encapsulated human mesenchymal cells producing glucagon-like peptide 1 prolongs survival in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/22745655

Intraspinal injection of human umbilical cord blood-derived cells is neuroprotective in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22122965

Intrathecal transplantation of human neural stem cells overexpressing VEGF provide behavioral improvement, disease onset delay and survival extension in transgenic ALS mice. http://www.ncbi.nlm.nih.gov/pubmed/19626053

Intravenous mesenchymal stem cells improve survival and motor function in experimental amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/22481270

Mesenchymal stromal cells prolong the lifespan in a rat model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/21736505

Minimally invasive transplantation of iPSC-derived ALDHhiSSCloVLA4+ neural stem cells effectively improves the phenotype of an amyotrophic lateral sclerosis model. http://www.ncbi.nlm.nih.gov/pubmed/24006477

MR spectroscopy evaluation and short-term outcome of olfactory ensheathing cells transplantation in amyotrophic lateral sclerosis patients. http://www.ncbi.nlm.nih.gov/pubmed/17305006

Multiple administrations of human marrow stromal cells through cerebrospinal fluid prolong survival in a transgenic mouse model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/19333801

Multiple intravenous administrations of human umbilical cord blood cells benefit in a mouse model of ALS. http://www.ncbi.nlm.nih.gov/pubmed/22319620

Neural stem cells LewisX+ CXCR4+ modify disease progression in an amyotrophic lateral sclerosis model. http://www.ncbi.nlm.nih.gov/pubmed/17439986

Positive effect of transplantation of hNT neurons (NTera 2/D1 cell-line) in a model of familial amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/11922659

Safety and immunological effects of mesenchymal stem cell transplantation in patients with multiple sclerosis and amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/20937945

Short-term outcome of olfactory ensheathing cells transplantation for treatment of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17933231

Stem cell transplantation in amyotrophic lateral sclerosis patients: methodological approach, safety, and feasibility. http://www.ncbi.nlm.nih.gov/pubmed/23356668

Stem cell treatment in Amyotrophic Lateral Sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/17582439

Stem-cell transplantation into the frontal motor cortex in amyotrophic lateral sclerosis patients. http://www.ncbi.nlm.nih.gov/pubmed/19191058

Systemic transplantation of c-kit+ cells exerts a therapeutic effect in a model of amyotrophic lateral sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/20650960

Systemic treatment with adipose-derived mesenchymal stem cells ameliorates clinical and pathological features in the amyotrophic lateral sclerosis murine model. http://www.ncbi.nlm.nih.gov/pubmed/23727509

Transient recovery in a rat model of familial amyotrophic lateral sclerosis after transplantation of motor neurons derived from mouse embryonic stem cells. http://www.ncbi.nlm.nih.gov/pubmed/19660174

Transplantation of human adipose tissue-derived stem cells delays clinical onset and prolongs life span in ALS mouse model. http://www.ncbi.nlm.nih.gov/pubmed/24070071

Treatment of amyotrophic lateral sclerosis patients by autologous bone marrow-derived hematopoietic stem cell transplantation: a 1-year follow-up. http://www.ncbi.nlm.nih.gov/pubmed/19012065