(140) Another assault drying agent been happening more and more lately.

perrin41@aol.com 

From:perrin41@aol.com

To:PERRIN PEREZ

Thu, Dec 4 at 5:47 AM

Asking the question: is someone with ventral medial frontal cortex damage more prone to parkinson's disease due to low dopamine levels resulting from lack of positive reinforcement due to complications with ventral medial frontal cortex damage?

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AI Overview

+12

There is 

no evidence to suggest that damage to the ventromedial prefrontal cortex (vmPFC) causes or increases a person's risk of developing Parkinson's disease (PD). 

Parkinson's disease is a neurodegenerative disorder primarily caused by the progressive loss of dopamine-producing neurons in the substantia nigra pars compacta (SNpc), a region in the midbrain, for reasons that are largely unknown (likely a combination of genetic and environmental factors). The vmPFC is a separate brain region involved in decision-making, reward processing, and social behavior, and while it receives dopaminergic innervation, its primary function is distinct from the core pathology of PD. 

Here is a breakdown of the relationship between the vmPFC, dopamine, and PD:

• Parkinson's Disease Pathology: The hallmark of PD is significant degeneration of the dopaminergic neurons in the SNpc, which primarily affects the nigrostriatal pathway responsible for motor control. This results in the characteristic motor symptoms of PD (tremor, stiffness, etc.).

• Dopamine and the vmPFC: The vmPFC receives dopamine input via the mesocortical dopamine pathway. Dopamine signaling in the vmPFC is involved in processing reward, effort, and social behavior. Damage to the vmPFC can lead to impairments in decision-making and apathy, which are non-motor symptoms that can also be seen in PD patients.

• Relationship between PD and the vmPFC:

  • PD itself can lead to dopamine depletion within the frontal cortex and affect vmPFC function as the disease progresses.

  • Apathy in PD is often associated with abnormalities in prefrontal cortical circuits, including the vmPFC.

  • Dopaminergic medications used to treat PD symptoms can modulate activity in the vmPFC.

• Risk Factors: The risk of developing PD is associated with factors like genetics, age, and environmental exposures, not primary damage to the vmPFC. 

In summary, damage to the vmPFC is a consequence or a related symptom of PD progression in some cases, but it is not an initial cause of the disease itself. The primary cause is the degeneration of dopaminergic neurons in the substantia nigra. 

Perrin take on this.

in some cases yeah like those with vmPFC damage have low dopamine baselines due to a lack of reinforcement that is actually self reinforcing at the neural level. Then overstimulated dopamine circuitry through adverse behaviors that become addictions and more extreme overtime. Dopamine has a fail safe mechanism that when blugeoned like in the circumstance in which I speak then dopamine will not downregulate so it will not replace therefore experiencing reward deficiency syndrome. This has everything to do with the substantia nigra. dopamine. And highly correlated to the underlying conditions that are understood that make up and the symptoms connected to this disease.  Which it would be fool hearted to neglect  how motivational states, behavior personality that contribute to vmPFC damage also contribute to the factors that can increase the risk of a person becoming afflicted by a symptoms of parkinsons and contracting the disease itself.

Also. Development and lack thereof yet connected to stress and not adapting well due to stringent harsh environments in early life and all throughout life but especially early on will a person's pathway not experience development of crucial circuitry  that is an important part of what is needed for a person to not experience vmPFC damage.

I am even though thd AI description fails to fully account for the biopsychosocial link  of development. For example, affect, mental experceives, are actually connected to  biological processess. Nevertheless, these biological processes can be afflicted in ways from development and how someone has evolved to function in specific ways that inhibit homeostasis in ways that lead of to negatively to neural structure that over time in functiong in this p a stern of behavior can contribute to and lead to multiple etiology. For example, in the case of negativel development experience as apathy, lack of moral reasoning hence the disconnect that leads to vmPFC damage therefore focus outward negatively in life never any form of positive reinforcement  that would be self reinforcing at the neural level therefore low dopamine baselines due to inactivity of the substantia nigra just like in parkinsons. Nonetheless I explained above the extremism that persists related to neural auctioning that evolves that can be explained by the maladaptive stress response and the dopamine serotonin hypothesis.

Stomach was feeling a bit blah and woke up in the middle of the night. Was looking at a some Instagram of Mr. Luna and seen him going to salute a female cadet in an academy class and what appeared to be his hand shaking at his side before doing do. Made me think do that's what I did and here's what I came up with. Cool Hugh. Well like anything it offers a hint of antidote  possibilities and that lifestyle changes could even halt the progression of disease. One hint apathy is part of vmPFC damage which is also a symptom of pakinsons. Maybe integrating a little love rather than hate in your life would help you out challenge before the end of the year. You think that you could do it even if it could help prevent a nasty disease? The balls in your court champ.