he has the most beautiful eyes, I wish him and his family the best, he is very brave

Such a brave young man. I pray for a cure. Huntingtons Desease took my first and forever love from me. I miss him so very much. Huntingtons can't take the beautiful memories i have.

I'm so proud of HDYO, Wayne and all the young people in these videos that opened up and shared this invaluable information with the world!!!!

Another lovely guy I met in 2011 & still keep in touch with. Yes he does have beautiful eyes but also such a great sense of humour & it's a pleasure to have spent time with Wayne and Matt when they were here in Australia.

Live a life and be proud of who you are because I don’t know you and I’m proud to be a part of your journey and that you have the courage to get tested and to share your story. I made a vow to stop whining since seeing quite a number of HD sufferers share their stories. I’m much more aware and thankful to the people like yourself in the videos for helping me understand. Thank you for this privilege.

keep that hope ! life could still be meaningful if we grasped the moment to the utmost, love our family

Thank you for your openness. I appreciate it.

God bless you, Wayne!!!

Having received a positive cancer diagnosis at age 22,I can RELATE. When you're so very young like that, you really do envision your entire long life ahead of you, even if you have entertained thoughts of an early demise... NOTHING can prepare you for the sinking feeling of your utter mortality smacking you in the face. It's all TOO REAL and very SURREAL all at once.

Hugs to you, you are v brave, thank you so much for sharing

Bless you Wayne xx

Here goes, Posting this here because I know some of you do research and think I may have stumbled upon a very important insight concerning the etiologies of various neurodegenerative disorders and maybe degenerative disorders in general. I’ll cut to the chase and ask the question and then explain how I got to the hypothesis. It is: Is it possible that distinct neurodegenerative and musculoskeletal degenerative disorders are in fact be specific symptom complexes that correspond to dysfunction of specific substructures of the cervical ganglia which subsequently alter certain functionalities of the choroid plexus and have downstream effects on the basal ganglia and spine? A recent medical situation in my life prompted me to conduct some personal research to better understand my condition. As a result, I became familiarized with the dynamics of a specific system of structures in the body that, if better understood and regarded as a unified whole, could potentially shed a brighter light in the etiologies of degenerative disorders. Essentially, my research led to make connections between three structures in the neck and head: the cervical ganglia, the choroid plexus, and the basal ganglia. A few observations became key in developing this idea about cervical ganglia involvement in degenerative disease. The first had to do with the basal ganglia. Basal ganglia dysfunction can cause a dearth of dopamine in the brain and subsequent cluster headaches and Parkinsonism/movement disorder symptomatology. This structure controls voluntary movement in the body and so in the case of movement disorders, it is usually the culprit. The question then becomes what is the fundamental cause of this dysfunction? jamanetwork.com/journals/jamaneurology/fullarticle/784785 Thinking about a specific syndrome called Eagle’s Syndrome which often presents with symptomatology similar if not identical to that of neurodegenerative/movement disorder. Eagle’s Syndrome is an abnormal ossification and elongation of the styloid process at the base of the skull that interferes with the cervical ganglia and carotid arteries in the neck and creates symptoms. actascientific.com/ASDS/pdf/ASDS-02-0202.pdf I wondered if superior cervical ganglia dysfunction could have downstream effects on the basal ganglia and cause disorder. So I began to attempt to understand the dynamic relationship between the cervical and basal ganglia. I began to look more closely at the cervical ganglia, in particular the superior cervical ganglia. This structure innervates the eye, parts of the face, the throat and sinuses, stimulates mucous production, has a part in regulating heartbeat (an aside: the disruption of the cervical ganglia when an Eagle’s Syndrome sufferer turns their head can result in panic symptoms: palpitations, dry mouth, gagging, so this could be a tool when thinking about mental heath physiopathologies as well), and also found that it is the only peripheral structure that sympathetically innervates areas of the head and brain. In particular, it innervates a structure in the brain called the choroid plexus. This was the next bridge on my way to the basal ganglia. en.wikipedia.org/wiki/Superior_cervical_ganglion The choroid plexus and found that it has a few very important functions: 1. To release transferrin that promotes iron homeostasis in the brain 2. Send agents to bind with antibodies to be flushed out of the system when infections are resolved and 3. Stimulate production of cerebrospinal fluid. That all struck me as fairly promising. en.wikipedia.org/wiki/Choroid_plexus I started with antibodies and found articles about post-infection movement disorders (specifically PANDAS, about which there is now literature about non-pediatric cases) where it is shown that sufferers have anti basal ganglia antibodies. www.ncbi.nlm.nih.gov/books/NBK333433/ It struck me that if a substructure of the cervical ganglia that innervates parts of the choroid plexus that promote production of antibody binding agents is dysfunctional, an infection could very well trigger an indefinite autoimmune response, attacking the basal ganglia and other systems. Some neurodegenerative and degenerative disorders like MS are thought to be autoimmune, and disruption of the cervical ganglia and subsequent introduction of infection could precipitate an indefinite autoimmune response. Symptom progression might depend on the nature of the ganglia dysfunction (if it is ongoing, say, due to injury and resulting occlusion, or intermittent, say, due to Eagle’s Syndrome, in which turning the head causes ganglia disruption), theoretically accounting for the different subtypes of MS. www.nationalmssociety.org/What-is-MS/Definition-of-MS/Immune-mediated-disease I also had the thought that if iron deregulation in the brain could be caused by dysfunction of a specific substructure of the cervical ganglia and subsequently the choroid plexus, maybe iron irregularities in the basal ganglia would be observed in sufferers of movement disorders, and sure enough, it’s observed in most, if not all of them. At this point I felt like I was really onto something. www.ncbi.nlm.nih.gov/m/pubmed/22266337/ And then a thought occurred to me: what if the first domino to fall in the etiologic chain of ALL of these degenerative disorders begins in the cervical ganglia? This could be why there are peripheral nervous system symptoms that manifest early in diseases like MS (the cervical ganglia innervates the eye and throat and heart, so vision dysfunction, dysphasia, heart rhythm problems etc would be some of the first symptoms you’d expect to see in this etiologic formulation). I’d seen papers talk about a corticothalamic basal ganglia circuit, but not much of anything about the cervical ganglia or choroid plexus, and I thought, “maybe the cervical ganglia is part of that circuit, affecting it indirectly but very profoundly.” Not everyone who suffers from degenerative diseases would have Eagle’s Syndrome of course, but maybe there would be occlusion/tortuosity of the ECA or cervical ganglia, or maybe a trauma shifted their positions leaving the cervical ganglia susceptible to injury, or maybe genetic degenerative disorders’ gene expressions simply omit instructions for certain substructures of the cervical ganglia to form and subsequently instruct the choroid plexus. So the idea is, if there are three main tasks of the choroid plexus, then there are seven combinations of those tasks (1; 2; 3; 1+2; 2+3; 1+3; and 1+2+3), and there are two ways for each of those tasks to dysfunction (over-firing or under-firing, although I’m not exactly sure about this detail), then each combination of simultaneous or sole dysfunction of cervical ganglia substructures which correspond to areas of the choroid plexus that are involved with completion of one of these three tasks would represent a distinct symptomatology-i.e., a distinct degenerative disorder. Important to note is that for antibody binding dysfunction due to lack of transferrin to become part of a neurodegenerative symptom complex, it may require an initial infection of a certain type to kick-start an autoimmune response strong enough to manifest in this way. In my reading about PANDAS I came across mention of “molecular mimicry,” and I thought maybe it was possible in the case of infections that feature such molecules, and in patients that have cervical ganglia dysfunction, that since the infection that the immune system (now totally unchecked by transferrin-aided antibody binding) is targeting resembles healthy structures in the body that all of these factors compounded could lead to ongoing destruction of healthy body tissue. It may be the case that I’m off base, or there are ways to easily prove false all that I’ve said, but I don’t know that. That’s why I’m posting, because in the unlikely event that this is not totally crazy, and might actually be plausible, it will be in the hands of people who can do something with it. A theory is judged by its explanatory power, and to me, this one seems to explain a lot. Could it be the skeleton key that unlocks understanding of these diseases and leads to new treatments and potentially cures? Is it simply that the cervical ganglia needs to be attended to more intensively when these disorders manifest? According to the literature, somewhere between 80-95% of Eagle’s Syndrome patients who undergo styloidectomies have complete cessation of symptoms. If I am right about the cervical ganglia’s role in degenerative disorders, and some of these patients’ styloid process was in contact with their ECAs and cervical ganglia, the neurological symptomatologies that presented may well have progressed into full-blown neurodegenerative disorder if left unaddressed. It could very well be the case that these successful surgeries represent instances of the curing of previously thought to be incurable neurodegenerative conditions. But again, Eagle’s syndrome merely represents one mechanism of action that could cause cervical ganglia dysfunction. I’d appreciate any response, even if it’s to tell me why I’m off base. I hope you’ve read with an open mind, and were willing to ask yourself “what if?” So, the question is: is it possible that superior ganglia dysfunction is the primary etiological feature of a host of neurodegenerative disorders? That this could be a unifying theory?

When will there be a cure for this horrendous disease?I believe it is getting closer and I so hope it comes in time for all these lovely young people who must be really frightened about their futures.good luck to all of them.

You are so brave 🙏🏽❤️

i have people in my family who think that if i say an opinion it doesn't 'count' if they disagree because i 'have hd'.

My 55 year old father was diagnosed with HD 3 days ago, since then my life is basically at a standstill. I am so afraid to carry this defective gene, i'm trying not to think about it, but it's haunting. I do not want to do this test to be honest. I'm not sure how I will take the result. I am currently 26 years old and I hope that I can give this a place.

My dad just tested positive

Isn't he beautiful 😻.. 🤗😄😉

Good luck to you man. The yin yang thing really owes you something :/

You are a beautiful person. Please know that Jesus is in charge, and you will be fine. He will take care of you. 💜❤️💙💜❤️💙💜❤️💙💜❤️💙

Awwwww☹💔

genetic counsellor

Has anyone else noticed that a large number of people who test positive have those same green eyes?

WWJD - What would Jesus do?