Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, March 10, 2025

Leptin as a potential neuroprotective target in Parkinson’s Disease: Exploring its role in Neuroinflammation, oxidative Stress, and dopaminergic neurodegeneration

 What does your competent? doctor think of this as a preventive for your risk of Parkinsons post stroke? Or does your doctor not follow research at all and thus doesn't need to think past med school?

Do you prefer your doctor and hospital incompetence NOT KNOWING? OR NOT DOING?

The latest here:

Leptin as a potential neuroprotective target in Parkinson’s Disease: Exploring its role in Neuroinflammation, oxidative Stress, and dopaminergic neurodegeneration

a ∙ b ∙ a bishalarann@gmail.com
  • Cite

    • Highlights

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    Leptin receptors in the substantia nigra and hippocampus play a key role in dopaminergic neuron survival.
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    Leptin protects against PD by activating JAK2/STAT3 and PI3K/Akt pathways, reducing neuroinflammation and oxidative stress.
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    Leptin holds promise as a therapeutic target to enhance neuroprotection and clinical outcomes in PD.

    Abstract

    Parkinson’s disease (PD) is the second most commonneurodegenerative disease, characterized bybradykinesia, resting tremor, stiffness, and postural instabilityresulting due to the progressive loss ofdopaminergic neurons in the substantia nigra (SN). The pathophysiology of PDis extremely complex and involves mitochondrial dysfunction, oxidative stress, neuroinflammation, and disruption of protein homeostasis. Its progression is affected by both environmental and genetic factors, including mutations in the alpha-synuclein (SNCA), PTEN-induced kinase 1 (PINK1), and leucine-rich repeat kinase 2 (LRRK2) genes. Leptin, primarily secreted by the adipose tissue, has garnered significant interest for its involvement in neuroprotective mechanisms and potential role in the progression of PD. Its receptors located in the SN and hippocampus region indicate its role in neuronal survival and function. The role of leptin in the central nervous system (CNS) highlights its impact on neuroinflammation, oxidative stress, and synaptic plasticity. Recent studies indicate that through activation of Janus kinase/signal transducer and activator of transcription (JAK2/STAT3) and the phosphoinositide 3 kinase (PI3 K)/Akt pathways, leptin may exert a neuroprotective effect by preventing the degeneration of dopaminergic neurons, which marked as the hallmark in the pathophysiology of PD. Additionally, leptin’s interaction with neurotrophic factors and its ability to enhance synaptic plasticity highlight its vital role in preserving neuronal health. This review summarizes the role of leptin as a neuroprotective mechanism in PD and explores its potential role as a therapeutic target for treatment to enhance neuroprotection and clinical outcome, by addressing the neurodegenerative characteristics associated with PD.
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