4 ms·

First line of the abstract of the paper: >Recent evidence suggests neurogenesis is on-going throughout life but the relevance of these findings for neurodegene

First line of the abstract of the paper: >Recent evidence suggests neurogenesis is on-going throughout life but the relevance of these findings for neurodegenerative disorders such as Parkinson’s disease (PD) is poorly understood.

aantix 6y ago
I've been taking magnesium l-threonate and l-theanine before bed, I seem to have more dreams and more intense dreams. I've seen both linked to neurogenesis. Is Mg deficiency part of the issue? https://www.ncbi.nlm.nih.gov/books/NBK507269/#_ch17_Low_Mg_and_Parkinson_s_disease_mode_ https://www.ncbi.nlm.nih.gov/books/NBK507269/#_ch17_Low_Mg_a...
- ipaddr 6y ago
  Mg threonine/ate usually is taken in the morning because it crosses the brain barrier causing an active response. I can see why you have active dreams. Try changing your mg type for less active nights.
gwerbret 6y ago
They are misrepresenting the state of knowledge in that field. It has indeed been known -- since the 90s -- that there is ongoing neurogenesis in the human brain after birth. However, it is also well-known that these new neurons are produced in regions of the brain that are not relevant to Parkinson's. The specific neurons that are lost in this disease, from a region of the brain known as the substantia nigra, are not normally replaced by ongoing neurogenesis. (I say "not normally" because redirecting neurogenesis to supply new neurons to the substantia nigra, as a treatment for Parkinson's disease, has been an ongoing area of research for decades.) Note also that this research study was done with zebrafish, whose neurobiology is dramatically different from humans.
- phcordner 6y ago
  This is also addressed in the paper: "Zebrafish are a particularly valuable tool to study neurogenesis in vertebrates. Basal levels of neurogenesis occur at higher levels than in mammals, and additional proliferative zones are found throughout the brain" In the zebrafish model, which yes, is different from the human brain, the researchers specifically demonstrate that neurogenesis is occurring in dopaminergic regions throughout life: "... we demonstrate that ascending TPp DA neurons and local-projecting PVO neurons, but not magnocellular ascending DA neurons, are each generated into adulthood in wild type animals at a rate that decreases with age." PINK1 deficiency slows the rate of the generation of DA neurons in zebrafish. Following this result, they then turned to the question of applicability to human systems by testing PINK1 deficiency on a culture of human midbrain organoids and successfully showed that this gene downregulated the size these organoids reached, demonstrating that this gene has an effect on neurogenesis of human dopaminergic neurons from the substantia nigra. "Isolated observations in animal models of PD always raise concerns about the applicability of any results to human patients with this condition. However, the observation of impairment of DA neurogenesis in a PINK1-deficient, human tissue derived organoid model confirmed the initial observations."
  - gwerbret 6y ago
    > demonstrating that this gene has an effect on neurogenesis of human dopaminergic neurons from the substantia nigra. But there is no neurogenesis of human dopaminergic neurons in the adult substantia nigra. To create the organoid model, they used fibroblasts to generate induced pluripotent stem cells, and then differentiated these into neurons in culture. As an experimental model, this is fine, but it is not particularly indicative of actual human biology. The most you could probably infer from this paper is that IF there were dopaminergic progenitors in the human substantia nigra (there aren't), they MIGHT respond this way if you deleted PINK1.
    - phcordner 6y ago
      In neurobiology, human in vivo studies are prohibitive from a cost, logistical, and ethical standpoint. But to anyone who can successfully parse a neurobiology paper this is assumed knowledge.

aantix 6y ago

I've been taking magnesium l-threonate and l-theanine before bed, I seem to have more dreams and more intense dreams. I've seen both linked to neurogenesis. Is Mg deficiency part of the issue? https://www.ncbi.nlm.nih.gov/books/NBK507269/#_ch17_Low_Mg_and_Parkinson_s_disease_mode_ https://www.ncbi.nlm.nih.gov/books/NBK507269/#_ch17_Low_Mg_a...

ipaddr 6y ago
Mg threonine/ate usually is taken in the morning because it crosses the brain barrier causing an active response. I can see why you have active dreams. Try changing your mg type for less active nights.

gwerbret 6y ago

They are misrepresenting the state of knowledge in that field. It has indeed been known -- since the 90s -- that there is ongoing neurogenesis in the human brain after birth. However, it is also well-known that these new neurons are produced in regions of the brain that are not relevant to Parkinson's. The specific neurons that are lost in this disease, from a region of the brain known as the substantia nigra, are not normally replaced by ongoing neurogenesis. (I say "not normally" because redirecting neurogenesis to supply new neurons to the substantia nigra, as a treatment for Parkinson's disease, has been an ongoing area of research for decades.) Note also that this research study was done with zebrafish, whose neurobiology is dramatically different from humans.

phcordner 6y ago
This is also addressed in the paper: "Zebrafish are a particularly valuable tool to study neurogenesis in vertebrates. Basal levels of neurogenesis occur at higher levels than in mammals, and additional proliferative zones are found throughout the brain" In the zebrafish model, which yes, is different from the human brain, the researchers specifically demonstrate that neurogenesis is occurring in dopaminergic regions throughout life: "... we demonstrate that ascending TPp DA neurons and local-projecting PVO neurons, but not magnocellular ascending DA neurons, are each generated into adulthood in wild type animals at a rate that decreases with age." PINK1 deficiency slows the rate of the generation of DA neurons in zebrafish. Following this result, they then turned to the question of applicability to human systems by testing PINK1 deficiency on a culture of human midbrain organoids and successfully showed that this gene downregulated the size these organoids reached, demonstrating that this gene has an effect on neurogenesis of human dopaminergic neurons from the substantia nigra. "Isolated observations in animal models of PD always raise concerns about the applicability of any results to human patients with this condition. However, the observation of impairment of DA neurogenesis in a PINK1-deficient, human tissue derived organoid model confirmed the initial observations."
- gwerbret 6y ago
  > demonstrating that this gene has an effect on neurogenesis of human dopaminergic neurons from the substantia nigra. But there is no neurogenesis of human dopaminergic neurons in the adult substantia nigra. To create the organoid model, they used fibroblasts to generate induced pluripotent stem cells, and then differentiated these into neurons in culture. As an experimental model, this is fine, but it is not particularly indicative of actual human biology. The most you could probably infer from this paper is that IF there were dopaminergic progenitors in the human substantia nigra (there aren't), they MIGHT respond this way if you deleted PINK1.
  - phcordner 6y ago
    In neurobiology, human in vivo studies are prohibitive from a cost, logistical, and ethical standpoint. But to anyone who can successfully parse a neurobiology paper this is assumed knowledge.