We have cured* Alzheimer's

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sincx: Jul 13, 2012; furiously masturbating to anime titties

* - potentially taken the first step towards curing

Still exciting nonetheless. New monoclonal antibody actually stimulates the body to remove the toxic misformed protein plaques that are thought to be the cause of the disease. This is the first treatment that actually could stop and reverse the disease instead of merely slowing it down.

Monoclonal antibodies are pretty amazing. In the last two decades humanity has acquired the technology to find and isolate custom molecules that target very specific substances, and then mass produce them (mass producing arbitrary amino acid sequences!). And then we use them to in effect direct our bodies naturally existing machinery to attack what we want them to attack. Sufficiently advanced technology, etc. etc.

Study:
http://www.nature.com/nature/journal/v537/n7618/full/nature19323.html

Commentary (quoted for plebs that don't have access to a Nature subscription):
http://www.nature.com/nature/journal/v537/n7618/full/537036a.html

quote:

Alzheimer's disease: Attack on amyloid-β protein

Eric M. Reiman

Nature
537,
36�37
(01 September 2016)
doi:10.1038/537036a

Published online
31 August 2016

An antibody therapy markedly reduces aggregates of amyloid-β, the hallmark protein of Alzheimer's disease, and might slow cognitive decline in patients. Confirmation of a cognitive benefit would be a game-changer. See Article p.50

It is 25 years1 since the amyloid-β (Aβ) protein was proposed as the trigger for a cascade of events in the brain that lead to Alzheimer's disease. A growing number of anti-Aβ treatments have been developed to short-circuit this cascade � and several are currently being evaluated in people who have already developed or are at risk of developing symptoms of Alzheimer's (https://www.alzforum.org/therapeutics). On page 50, Sevigny et al.2 report findings from an initial 12-month, placebo-controlled trial of the antibody aducanumab, which selectively binds to potentially harmful soluble and insoluble Aβ aggregates, respectively called Aβ oligomers and fibrils.

The trial was primarily intended to clarify the Aβ-fibril-reducing effects and safety of different aducanumab doses administered intravenously once a month. It involved people who had been diagnosed with mild cognitive impairment (non-disabling memory and thinking problems) or mild dementia (which did have a slightly disabling effect) due to Alzheimer's disease. Each of the participants also tested positive for Aβ in a positron emission tomography (PET) scan, indicating moderate to frequent build-up of fibril-containing plaques � a cardinal feature of the disease. The study was not designed to definitively address aducanumab's effect on cognitive decline.

Aducanumab treatment was associated with unusually striking, progressive, dose-dependent reductions in PET measurements of Aβ-plaque burden. Aducanumab was also presumed to bind to and remove harder-to-measure Aβ oligomers, which seem to accumulate at or near plaques and may be the more damaging of the two aggregates3. What's more, despite the relatively small number of study participants and the substantial extent to which the disease has progressed by the time people with Alzheimer's develop memory and thinking problems, exploratory analyses suggested that higher antibody doses and greater Aβ-plaque reductions were associated with slower cognitive decline. If these preliminary cognitive findings are confirmed in larger and more-definitive clinical trials, which are now under way, it would provide a shot in the arm in the fight against Alzheimer's disease and compelling support for the amyloid hypothesis.

The amyloid hypothesis contends that a 42-amino-acid form of Aβ (Aβ42) becomes harmful when, owing to its overproduction or reduced clearance from the brain, individual Aβ42 monomers come together in various numbers and conformations to form oligomers and fibrils. These Aβ42 aggregates trigger a cascade of neurobiological events, including: certain inflammatory responses; aggregation, phosphorylation and propagation of a protein called tau; and other neuronal changes. These events contribute to the formation of Aβ plaques and tau-containing tangles, loss of neurons and the synaptic connections between them, cognitive decline and disability, and other features of Alzheimer's disease (Fig. 1).

This hypothesis contends that increases in the amyloid-β 42 (Aβ42) protein trigger a cascade of events in the brain that lead to Alzheimer's disease. Under this hypothesis, individual Aβ42 monomers aggregate into damaging oligomers and fibrils in or near Aβ42 plaques. Aβ aggregates cause certain inflammatory responses. Through unknown mechanisms, these events lead to the aggregation, phosphorylation and propagation of tau, a protein that is associated with microtubules (pink and purple) and is the main constituent of harmful tangles. Affected neurons and synapses become dysfunctional and can die, leading to additional inflammatory responses. The progressive dysfunction, degeneration and loss of affected neurons and synapses is associated with cognitive decline, other symptoms of Alzheimer's disease and increasing disability. Sevigny et al.2 report that the Aβ-binding antibody aducanumab binds to, promotes removal and blocks accumulation of fibrils and oligomers.

Proponents of the amyloid hypothesis cite an abundance of supporting evidence1. Others note that the evidence is largely circumstantial, and that questions remain about the offending Aβ species and its effects. As such, they wonder whether Aβ42 accumulation is a consequence rather than an initiator of disease, and worry that anti-Aβ drug development might lead to a dead end. What will it take to confirm or refute the amyloid hypothesis once and for all?

Confirmation of this hypothesis will require definitive evidence that an anti-Aβ treatment can reduce cognitive decline in people affected by or at risk of developing Alzheimer's disease. Sevigny and colleagues' trial provides convincing evidence that aducanumab can enter the brain, target Aβ fibrils and substantially reverse plaque deposition � a major advance. But although the authors' additional cognitive findings are encouraging, they are not definitive. It would be prudent to withhold judgement about aducanumab's cognitive benefit until results from the larger trials are in. It will also be useful to see what can be learnt from large trials of other anti-Aβ treatments in the coming months and years.

Conversely, refutation of the amyloid hypothesis will require failure of anti-Aβ treatments to reduce cognitive decline in sufficiently large and suitably designed trials � not only in people with cognitive impairment due to Alzheimer's disease, but also in people without such impairment who have evidence of Aβ plaques, and even people without impairment who are at genetic risk of developing Alzheimer's but have little or no Aβ deposition. Several prevention trials using anti-Aβ treatments have started4, and more are on the way. Because abnormal Aβ build-up can begin more than two decades before the onset of memory and thinking problems5, having a drug such as aducanumab that substantially reverses pre-existing Aβ deposition might increase the chances of extinguishing the disease even after it has set in.

What accounts for aducanumab's unusually pronounced plaque-busting effects, even in small doses and despite the fact that only one to two antibody molecules out of every thousand are thought6 to cross the blood�brain barrier? It might be a combination of three things: the drug's unusually high selectivity for Aβ42 fibrils and oligomers, which minimizes the number of antibody molecules that bind to the abundant Aβ monomers in the blood and so maximizes the number of unbound antibodies that can enter the brain; its unusually high affinity for Aβ42 fibrils and oligomers; and the mechanism by which it enlists microglia, the brain's principal immune cells, to engulf and clear Aβ fibrils.

On the one hand, aducanumab's microglia-mediated activity could account for the antibody's ability to remove plaques, rather than just to slow further Aβ accumulation (which would be valuable in its own right). On the other hand, this activity might increase the chance of people developing amyloid-related imaging abnormalities (ARIA) � defects characterized by evidence of brain-fluid accumulation in magnetic resonance imaging scans. Like certain other anti-Aβ antibody treatments7, Sevigny and colleagues' study found that aducanumab was more likely to cause ARIA in higher doses and in people who carry the APOE type 4 gene, which is the major genetic risk factor for Alzheimer's disease.

The authors observed that ARIA were sometimes associated with transient headaches, visual disturbances or confusion, but were often associated with no symptoms, and that symptoms typically resolved within one to three months. Nonetheless, the frequency of ARIA caused the researchers to limit the maximum dose studied. It will be important to establish a sweet spot: a dose that is sufficiently safe and well tolerated, but also effective.

In addition to confirming the amyloid hypothesis, finding that the effects of treatments such as aducanumab on Aβ or other biological measurements of Alzheimer's disease are associated with a cognitive benefit might help to accelerate the evaluation and regulatory approval of promising Alzheimer's-prevention therapies that are based on reducing the biological measurements alone4. Indeed, confirmation that an anti-Aβ treatment slows cognitive decline would be a game-changer for how we understand, treat and prevent Alzheimer's disease. Now is the time to find out.

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# ? Sep 1, 2016 22:17

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# ? Apr 27, 2024 12:38

communism bitch: Apr 24, 2009

Can this cure the misformed protein in my cum op?

# ? Sep 1, 2016 22:18

AugmentedVision: Feb 17, 2011; by exmarx

I thought pot cured Alzheimer's

# ? Sep 1, 2016 22:18

Captain Yossarian: Feb 24, 2011; All new" Rings of Fire"

This is actually good news thanks for sharing op. In the spirit of kindness, I will wish you good health and positive vibes.

# ? Sep 1, 2016 22:20

VendaGoat: Nov 1, 2005

AugmentedVision posted:

I thought pot cured Alzheimer's

Dave's not here man.

# ? Sep 1, 2016 22:21

AugmentedVision: Feb 17, 2011; by exmarx

Imagine if your grandma got the placebo

# ? Sep 1, 2016 22:21

Principals Orifice: Aug 23, 2016; by Lowtax

hell I don't even remember ten minutes ago

# ? Sep 1, 2016 22:22

ROFLburger: Jan 12, 2006

suck my boner, op

# ? Sep 1, 2016 22:24

sofokles: Feb 7, 2004; Fuck this

Have I posted yet?

# ? Sep 1, 2016 22:25

Phlairdon: Apr 15, 2003; If you can't stand up you can't do war!

Not fast enough to save Gene Wilder and Terry Pratchett, but slow enough to kill of Reagan.

# ? Sep 1, 2016 22:25

reallivedinosaur: Jun 13, 2012; Ogdober subrise! XDDD

when are they going to cure "the common cold"

# ? Sep 1, 2016 22:26

ROFLburger: Jan 12, 2006

suck my boner, op

# ? Sep 1, 2016 22:26

Hector Beerlioz: Jun 16, 2010; aw, hec

AugmentedVision posted:

I thought pot cured Alzheimer's

It's actually the cause

# ? Sep 1, 2016 22:26

Principals Orifice: Aug 23, 2016; by Lowtax

ROFLburger posted:

suck my boner, op

lmao we'll played

# ? Sep 1, 2016 22:27

Mariana Horchata: Jun 30, 2008; College Slice

good, now i hope they cure parkinsons next since im prob gonna catch that and slowly die in sheer misery

also i hope George W Bush gets alzheimers tho and his brain turns to tapioca puddling just like Reagan as payback for his meddling with the use of stem cells when ppls lives could have been saved if not for his religious delusions and personal conversations with Jesus. rear end in a top hat

# ? Sep 1, 2016 22:27

CJacobs: Apr 17, 2011; Reach for the moon!

Good. My great grandma died of alzheimer's and it was very depressing to watch and I'm sure for her to experience, so I'm glad to see progress toward telling it to gently caress off it is being made.

# ? Sep 1, 2016 22:28

Kuato: Feb 25, 2005; "I CAN'T BELIEVE I ATE THE WHOLE THING"; Buglord

Please cure death next. I would like to be immortal. Spanks in Advance

# ? Sep 1, 2016 22:29

Instruction Manuel: May 15, 2007; Yes, it is what it looks like!

poo poo, hopefully it'll be ready by the time Alzheimer's strikes my own poo poo brain

lol just kidding, American healthcare :smithicide:

# ? Sep 1, 2016 22:37

Solice Kirsk: Jun 1, 2004; .

Too bad Neurimmune isn't on the stock market....

# ? Sep 1, 2016 22:38

sincx: Jul 13, 2012; furiously masturbating to anime titties

Wamdoodle posted:

lol just kidding, American healthcare

This is why:

Solice Kirsk posted:

stock market

# ? Sep 1, 2016 22:39

ElectricSheep: Jan 14, 2006; she had tiny Italian boobs.
Well that's my story.

i forgot the subject of OPs wall of text about three paragraphs in

# ? Sep 1, 2016 22:40

Bulgogi Hoagie: Jun 1, 2012; We

how super expensive is this monoclonal antibody going to be

# ? Sep 1, 2016 22:48

Moridin920: Nov 15, 2007; by FactsAreUseless

Lichy posted:

how super expensive is this monoclonal antibody going to be

lol

# ? Sep 1, 2016 22:49

VendaGoat: Nov 1, 2005

Lichy posted:

how super expensive is this monoclonal antibody going to be

Well, you asked, so that means you can't afford it.

# ? Sep 1, 2016 22:49

Solice Kirsk: Jun 1, 2004; .

sincx posted:

This is why:

Insurance is why, not the stock market. Similar though!

# ? Sep 1, 2016 22:51

signalnoise: Mar 7, 2008; i was told my old av was distracting

thats cool

# ? Sep 1, 2016 22:51

The Duchess Smackarse: May 8, 2012; by Lowtax

Lichy posted:

how super expensive is this monoclonal antibody going to be

10 bux for the first little while, and then some rear end in a top hat will buy the rights and it'll be 100,000,000 bux and you have to give 6 different big pharm lobbyists hand beezies

# ? Sep 1, 2016 22:51

shoophobo: Aug 30, 2013; "shoophobo? more like shittyposter!"; Fallen Rib

Modern Medicine is cool and good.
My dad is getting in a study to get some stem cell things in his busted rear end neck. So that's cool.
Thanks for sharing this news post op.

# ? Sep 1, 2016 22:52

sincx: Jul 13, 2012; furiously masturbating to anime titties

Lichy posted:

how super expensive is this monoclonal antibody going to be

Actually, if it's a cure, it'll be cheaper than providing decades of increasingly more complicated nursing home palliative care.

And there's a big enough market that after the patent expires, there should be generic competition, barring any senator's-daughter-type corruption. So assuming you aren't already old, it should be reasonable if you need it.

# ? Sep 1, 2016 22:52

Uncle Wemus: Mar 4, 2004

Now i can start smoking

# ? Sep 1, 2016 22:53

Solice Kirsk: Jun 1, 2004; .

If you're over 18 then you should have been smoking already. Only people that start smoking at like 12 live to see their 90's. If you start at like 18-20 then you die from horrible cancers in your 60's. If health was a serious concern the government would lower the smoking age.

# ? Sep 1, 2016 22:58

yogizh: Oct 12, 2015; Dumb Helicopter Joke Enthusiast

AugmentedVision posted:

I thought pot cured Alzheimer's

Yea it does, folks did that brainscan thingy with the same effect. Of course the industry needs something 20 times more complicated as an excuse for the pricing.

# ? Sep 1, 2016 23:00

whoflungpoop: Sep 9, 2004; With you and the constellations

AugmentedVision posted:

Imagine if your grandma got the placebo

# ? Sep 1, 2016 23:02

ColoradoCleric: Dec 26, 2012; by FactsAreUseless

I heard this poo poo causes brain swelling and bleeding

# ? Sep 1, 2016 23:39

penus penus penus: Nov 9, 2014; by piss__donald

Just floss

# ? Sep 1, 2016 23:48

Moridin920: Nov 15, 2007; by FactsAreUseless

just a reminder that the company that makes EpiPens, the poo poo you need to carry with you if you have a bad allergy so you don't literally die, cranked the cost to $600 a pair over the course of the last year or so.

They also awarded multi million dollar bonuses to executives for improving their revenues.

quote:

At the time, the bonuses were worth $82 million to its five top executives alone, according to The Wall Street Journal.

quote:

At drug price-comparison website GoodRx, the cheapest price today is $614 for a package containing two, or more than $300 per EpiPen, up from about $100 for two.

Meanwhile kids with bad allergies can just deal with it lmao

but but but we gotta pay for research

quote:

After years of price hikes, revenue has surged to about $1 billion annually. Margins have jumped from about 9 percent in 2008 to about 55 percent in 2014, Bloomberg News reported, citing researcher ABR|Healthco

lol so what if some peanut kids suffocate gently caress 'em

# ? Sep 1, 2016 23:48

Skeleton Ape: Dec 21, 2008

AugmentedVision posted:

Imagine if your grandma got the placebo

Yeah, they should tell people in medical studies that there is no guarantee that this will work, it won't make things worse, or you will even be receiving the treatment. I can't believe they don't do that :mad: