u/MD_Ex

Mitochondria are far more than the “power plants” of our cells.

They regulate energy production, inflammation, oxidative stress, apoptosis, and cellular signaling. When mitochondrial function declines, cells lose their ability to repair, communicate, and survive under stress.

This is why mitochondrial dysfunction is increasingly recognized as a common denominator in many chronic and degenerative diseases, including cancer, Alzheimer, Parkinsons, epilepsy, stroke, cardiovascular disease, and age-related cognitive decline.

In cancer, damaged mitochondria can alter cellular metabolism and promote uncontrolled growth.
In neurodegenerative disorders, neurons—among the most energy-demanding cells in the body—become highly vulnerable when mitochondrial ATP production falls.
In stroke and ischemic injury, mitochondrial failure triggers cell death cascades and worsens tissue damage.

Research into mitochondrial transfer, mitophagy enhancement, NAD+ restoration, stem cell–derived exosomes, and targeted metabolic therapies may open entirely new approaches for diseases once considered irreversible.
It may be the key to unlocking treatments for some of the most devastating diseases of our time.

I work in regenerative medicine, and in discussions around stem cell therapies for diseases like ALS, Parkinson’s, and MSA, one thing keeps coming up again and again: the source of the cells really matters.
At this stage, most treatments are not aimed at curing these diseases, but rather at slowing progression and supporting the survival of remaining nerve cells.

In practice, there is an important difference between two main approaches.
Autologous cells are taken from the patient’s own body (for example bone marrow or fat tissue). In theory, this sounds ideal because the body should “recognize” its own cells. However, in neurodegenerative diseases, these cells often already reflect the patient’s condition. They may be less active, less efficient, broader age- or disease-associated epigenetic drift. ( as the carrier of all our cellular damages)
This can make their effect less consistent.
Allogeneic cells come from healthy donors. These cells are generally younger, more active, and more standardized. Because they are produced from healthy sources, their quality and behavior tend to be more consistent across batches, which is important in clinical development.

There are also different types of stem cells being studied:
Mesenchymal stem cells are the most commonly used today. They do not usually replace nerve cells directly, but they can reduce inflammation and send signals that help support tissue repair.
Neural stem cells are closer to actual brain and nerve cells, so they are more directly related to repairing the nervous system. However, they are still difficult to produce and use on a large scale.
Induced pluripotent stem cells (iPSCs) are one of the most advanced approaches. These cells can be guided to become specific types of nerve or support cells. This gives a lot of control and precision, but also makes the process more complex and carefully regulated.

Overall, the field is moving away from a “one cell fits all” idea. Instead, the focus is shifting toward using better-defined, more consistent, and more precisely designed cell products.
What do you think about it?

There’s growing interest in regenerative approaches for improving ovarian reserve and ovarian aging, usually using mesenchymal stem/or combination with exosomes or PRP .

What current studies and clinical observations speak about :

MSC-based therapies appear to act primarily through paracrine signaling,
Reported effects in clinical studies and case series include:

1. improvement in ovarian reserve markers (e.g., AMH, AFC in some patients)
   2)recruitment or activation of residual dormant follicles
2. improved ovarian microenvironment (“niche”), including:
   angiogenesis
   reduced local inflammation
   mitochondrial support via extracellular vesicles
   Exosomes and mitochondrial transfer mechanisms are being actively studied for their role in:
   cellular metabolism
   granulosa cell function
   follicular survival

In simple words : therapy may help optimize the use of the remaining follicular pool, rather than create new eggs.

What this therapy does not currently do:

1. It does not reverse the biological age of the oocyte. It’s very important when the patient is 40+
2. It does not correct chromosomal abnormalities (aneuploidy)
3. It does not eliminate accumulated DNA mutations
4. It cannot reliably “improve egg quality” in the genetic sense

Stem cell–based therapies may offer a way to enhance ovarian function and recruit remaining follicles, but they do not reset ovarian aging at the genetic level.

So realistic expectation is functional** **support - quantity, but not biological rejuvenation of oocyte quality.

If somebody tried similar treatments, I would be great to read about your results

Sharing an anonymized clinical observation for academic discussion.

Patient: male, 35 years old

Condition: chronic low back pain with MRI-confirmed L4–L5 disc degeneration

Baseline MRI findings:

Disc dehydration at L4–L5

Disc-osteophyte complex

Posterior disc extrusion causing deformation of the dural sac

No severe canal stenosis

Therapeutic approach (multimodal regenerative protocol):

The intervention included a combination of biologically active cellular components aimed at modulating inflammation and tissue microenvironment:

Endothelial cell cultures (vascular / microcirculatory support focus)

Neural lineage–derived cells (neuro-supportive / trophic signaling hypothesis)

iPSC-derived chondrocyte-like cells (disc matrix / cartilage-like ECM support)

The rationale was to target different components of the disc microenvironment (vascular, neural, and extracellular matrix signaling).

Follow-up imaging:

No clear evidence of disc extrusion on repeat MRI

Mild posterior disc bulging at L4–L5

No significant neural compression

Spinal canal remains patent

Clinical context:

The patient reportedly experienced symptom improvement alongside imaging changes.

Discussion point:

This single case raises questions about potential synergistic effects of multimodal cell-based approaches on disc inflammation, extracellular matrix remodeling, and local microenvironment regulation.

Would be interested in thoughts from other patients who used similar therapy about their experiences.