Shwe Parami Stroke Rehabilitation Clinic

06/12/2025

အိုမင်းခြင်းကိုမဖြစ်အောင် မိုက်တိုခွန်ဒရီးယားကောင်းမွန်သည့်အခြေအနေအပေါ်ပစ်မှတ်ထားသည် စီမံချက်မဟာဗျူဟာများ
၁၊ ကောင်းမွန်သော မိုတိုခွန်ဒရီးယားအသစ်များဖြစ်ပေါ်အောင်လှုံဆော်ခြင်း (biogenesis)
၂၊ ပျက်စီးသွားသည်မိုက်တိုခွန်ဒရီးများကိုရှင်းလင်းခြင်း (mitophagy)
၃၊ အင်တီအောက်စီဒင့်ကုထုံး (antioxident therapy)
၄၊ မိုက်တိုခွန်ဒရီးယားအစားထိုးခြင်း
(mitochondrial transplantation)
၅၊ ပြင်းအာနည်းလေဆာ သို့မဟုတ် အနီအောက်ရောင်ခြည် (low level laser or) infra red) တိုကို အသုံးပြုကုသပေးခြင်း (Photobiomodulation)
၆၊ မိုက်တိုခွန်ဒရီးယားသို့ ဆေးဝါးပို့ဆောင်ပေးခြင်း (drug delivery)
၇၊ လူနေမှုပုံစံ နှင့် အစားအသောက် (life style diets) တို့ဖြစ်သည်

Ant-aging Strategies Focus On Targeting Mitochondrial Health

Mitochondrial dysfunction is a core hallmark of aging, creating a vicious cycle where declining mitochondrial efficiency leads to increased cellular damage, energy deficits, and oxidative stress, accelerating the aging process and contributing to age-related diseases like neurodegeneration, metabolic syndrome, and cardiovascular issues.

This dysfunction involves decreased ATP production, elevated Reactive Oxygen Species (ROS), mitochondrial DNA mutations, impaired mitophagy (quality control), and disrupted calcium balance, ultimately causing systemic deterioration and increased disease risk.

Mitochondrial Dynamics: Imbalances in fission (splitting) and fusion (joining) affect mitochondrial size, number, and function.

DNA Damage: Accumulation of mutations and deletions in mitochondrial DNA (mtDNA) compromises function.

Vicious Cycle of Aging
Initial Damage: Aging stressors (like ROS) damage mitochondria.
Reduced Function: Damaged mitochondria produce less energy and more ROS.
Worsened Damage: Increased ROS causes more mtDNA/protein damage.
Systemic Decline: Cellular dysfunction spreads, impacting tissues and organs,
leading to age-related pathologies.

Associated Age-Related Conditions
Neurodegenerative diseases (e.g., Alzheimer's, Parkinson's)
Metabolic syndrome and Type 2 Diabetes
Cardiovascular diseases (e.g., atherosclerosis, hypertension)
Cancer
Sarcopenia (age-related muscle loss)

Key targeting mitochondria health
strategies include promoting
mitochondrial biogenesis,
removing damaged mitochondria through mitophagy, and
developing specific molecules to improve function or deliver antioxidants directly to the mitochondria.

Promoting : Strategies aim to stimulate the creation of new, healthy mitochondria.

Enhancing : Therapies can encourage the removal of damaged mitochondria, a process called mitophagy.

therapies: Molecules can be designed to target the mitochondria to combat oxidative stress. Examples include compounds conjugated with lipophilic cations.

: This is a novel approach being explored for certain conditions, such as bone diseases.

: This is another emerging strategy, particularly investigated for bone and cartilage health.

delivery: Researchers are creating novel methods, including using liposomes and other delivery systems, to deliver therapeutic agents specifically to the mitochondria.

Lifestyle and diet
Exercise: Aerobic exercise can increase mitochondrial density and improve their function.
Dietary Interventions: Diets like the ketogenic diet may support mitochondrial health.
Supplementation: Certain supplements such as CoQ10, B vitamins, and omega-3 fatty acids may support mitochondrial function.

Important considerations
Mitochondrial dysfunction is linked to a wide range of diseases, making targeting mitochondria a promising therapeutic avenue for many conditions.
Research is ongoing to understand and develop these strategies, with many molecules in development and clinical trials.

Photo credit

05/12/2025

Antiaging Strategies Focus on
Nutrient-Sensing Pathways (mTOR, AMPK)

Target strategies for cellular aging involve addressing hallmark processes like genomic instability, cellular senescence, and mitochondrial dysfunction
by promoting DNA repair,
eliminating senescent cells, or restoring mitochondrial health.

Key pathways to target include nutrient-sensing pathways (mTOR, AMPK), DNA damage response, and chronic inflammation, with interventions like pharmaceuticals (rapamycin, senolytics), lifestyle changes (diet, exercise), and naturally derived compounds showing promise in recent research.

Nutrient-sensing pathways like mTOR (promotes growth) and AMPK (conserves energy) are key regulators of aging, and anti-aging strategies focus on balancing their activity.
These pathways are tightly interconnected, integrating signals from nutrients, hormones, oxygen, and stress to maintain cellular homeostasis.
Strategies to promote longevity involve mTOR and AMPK through lifestyle choices like
restriction,
fasting, and exercise,
as well as through potential agents like rapamycin and metformin.

The mTOR signaling pathway is a central cellular pathway that integrates environmental signals, such as nutrients, growth factors, and energy, to regulate crucial cellular functions like growth, metabolism, proliferation, and survival. It does this by controlling processes like protein and lipid synthesis, autophagy, and mitochondrial function. The pathway functions through two main complexes, mTORC1 and mTORC2, which are activated by upstream signals like the PI3K/AKT pathway or phosphoinositide 3-kinase/protein kinase B pathway.
Dysregulation of the mTOR pathway is linked to several diseases, including cancer, type 2 diabetes, obesity, and neurodegenerative disorders.

The AMPK pathway is a cellular energy sensor that regulates metabolism in response to low energy levels by activating ATP-producing pathways and inhibiting ATP-consuming ones. It is a crucial signaling pathway that senses energy stress from low glucose or other factors, and in response, it promotes catabolic processes like fatty acid oxidation while suppressing anabolic processes like protein and lipid synthesis to restore energy balance. This makes it a key target for treating metabolic diseases such as diabetes, obesity, and cancer.

Rapamycin, also known as sirolimus, is an immunosuppressant drug and *mTOR
(Mechanistic target of rapamycin)
inhibitor used to prevent organ transplant rejection, treat lymphangioleiomyomatosis, and is being studied for its anti-aging effects and role in cancer therapy and drug-eluting stents.

Metformin: A common drug for type 2 diabetes that activates AMPK and has potential anti-aging properties.

03/12/2025

#အိုမင်းခြင်း နှင့်
#မအိုမင်းစေရန် အိုမင်းခြင်းကိုဖြစ်စေသော ဒီ အင် (န်) အေ ပျက်စီးစေခြင်း ကြောင့်ဖြစ်သောတုန်ပြန့်မှု နှင့် အိုမင်းခြင်းတွဲဖက်ဖြစ်သောဖီနိုတိုက်စိမ့်ထွက်ခြင်း (SASP) ကိုပစ်မှတ်ထား၍ စီမံချက်မဟာဗျုဟာများ

Aging and Anti-aging strategies targeting the DNA damage response (DDR) and
senescence-associated secretory phenotype (SASP)

Visible manifestations of aging encompass sensory decline (hearing loss, impaired vision), integumentary changes (skin sagging, increased wrinkles), diminished physical fitness and endurance, and gradual muscle weakening.

Cellular aging occurs through cell cycle arrest, which is the result of extended
DNA damage response (DDR) cascade signaling networks via MDC1, 53BP1, H2AX, ATM, ARF, P53, P13-Akt, BRAF, Sirtuins, NAD + , and so forth.

These persistent cell cycle arrests initiated by DDR and other associated stress-induced signals promote a permanent state of cell cycle arrest called senescence-associated secretory phenotype (SASP). However, cellular aging gets accelerated with faulty DNA repair systems, and the produced senescent cells further generate various promoting contributors to age-related dysfunctional diseases including SASP.

Senescence-associated secretory phenotype (SASP) is the secretion of a complex mix of molecules, including inflammatory cytokines, growth factors, and proteases, by senescent cells. This phenotype is a key driver of chronic inflammation and plays a crucial role in aging and age-related diseases, but can also contribute to initial tumor suppression by recruiting immune cells. Over time, SASP can also contribute to tumor growth by creating a pro-inflammatory environment that can fuel cancer development.

Anti-aging strategies targeting the DNA damage response (DDR) and SASP regulation pathway include pharmaceuticals, and natural compounds
(Examples of targeted factors are and , which can suppress SASP components like IL-6, and
and that interfere with inflammation pathways like NF-B.

Other strategies involve
enhancing DNA repair mechanisms
(Inhibiting DDR signaling, poly ADP-ribose polymerase (PARP) inhibitors) or developing senolytics (Examples include ABT-263, FOXO4-DRI, and BPTES.), drugs that eliminate senescent cells, to prevent the release of pro-inflammatory factors associated with the SASP.

Inhibiting DDR signaling: Targeting key kinases in the DDR pathway, such as the ATM-p53-p21 axis, can prevent senescence and mitigate age-related tissue damage.

PARP (poly ADP-ribose polymerase) inhibitors: These are used in cancer therapy to target DNA repair defects and are being explored for broader anti-aging applications.

Senolytics: Drugs that selectively kill senescent cells, which are cells that have stopped dividing due to DNA damage. (Examples include ABT-263, FOXO4-DRI, and BPTES.)

Regulating the SASP
Modulating SASP-inducing pathways:
NF-B and C/EBP inhibition: These transcription factors are central to the expression of SASP components.
Targeting upstream regulators: The mTOR, PI3K, and MAPK pathways can be targeted to indirectly control SASP.

Inhibiting the SASP
Mitochondrial targeting: Mitochondria play a key role in SASP development, and targeting them may offer a strategy to reduce detrimental SASP features.

Lifestyle interventions
Diet: Dietary changes, such as consuming flavonoids, can help mitigate oxidative stress, inflammation, and DNA damage.
Caloric restriction: Without full-scale calorie restriction, specific dietary restrictions can increase healthspan.

02/12/2025

CAR T-cell Therapy and CARs Generations

CAR T-cell therapy for cancer patients is an emerging form of immunotherapy. It involves supercharging a patient’s T cells so that they can recognize and attack cancer cells.

CAR T-cells are made by genetically engineering a patient's or a donor's T-cells.
To produce CAR-T cells, T cells are engineered with a chimeric antigen receptor (CAR) that includes an extracellular antigen-binding domain and an intracellular signaling domain, such as CD3-zeta (CD3ζ).

CAR-T cell design and function
Antigen recognition: An extracellular, single-chain variable fragment (scFv) derived from an antibody is used to bind to a specific antigen on the surface of a tumor cell.
Transmembrane domain: This part anchors the CAR in the T cell membrane, connecting the extracellular and intracellular components.
Intracellular signaling domain: This is the crucial part for T cell activation.

First-generation CARs: These only had the CD3ζ signaling domain to initiate T cell activation upon antigen binding.
Second- and third-generation CARs: These include one or two additional co-stimulatory signaling domains (e.g., CD28, 4-1BB) before the CD3ζ domain.

The CD3ζ chain is a key component of the endogenous T cell receptor (TCR) complex, which plays a critical role in transmitting the signal from antigen recognition to the inside of the T cell.
When the extracellular scFv binds to its target antigen, it causes a conformational change that activates the intracellular CD3ζ signaling domain.

The CD3 zeta (CD3ζ) chain is a protein component of the T-cell receptor (TCR)-CD3 complex, which is crucial for T-cell activation and adaptive immunity. It is encoded by the CD247 gene, is part of the CD3 complex along with the gamma, delta, and epsilon chains, and plays a vital role in transmitting signals from the TCR into the T-cell's interior.

The zeta chain is one of four proteins (gamma, delta, epsilon, and zeta) that, along with the TCR itself, form the complex on T-cells. Two zeta chains are linked together and also bound to other CD3 proteins.
It contains special motifs (ITAMs) that, once phosphorylated after TCR engagement, act as docking sites for other proteins, initiating a signal transduction pathway. This is crucial because the TCR itself cannot signal effectively due to its very short cytoplasmic tail.
The CD3ζ chain is critical for the proper assembly and expression of the TCR complex on the cell surface, which is necessary for the T-cell to recognize and respond to antigens.

Fourth-generation (4G) CAR T-cells, also called TRUCKs, are engineered to release transgenic cytokines such as IL-12, IL-15, or IL-18, upon activation to create a more favorable tumor microenvironment and enhance anti-cancer activity.

Fifth-generation CAR T-cells are an advanced form of CAR T-cell therapy these
include multiple intracellular signaling domains, allowing them to respond to a wider range of signals and pathways.
The incorporation of IL-2 receptor chain fragments enables antigen-dependent activation of the JAK/STAT pathway, which helps with T-cell proliferation and memory formation.
Some fifth-generation designs also incorporate the ability to secrete molecules like anti-PD-L1 antibodies, which can help overcome immune evasion mechanisms used by tumors.

Photo credit

28/11/2025

Cancer Therapy by Blocking Adenine Nucleotide Translocase-2 (ANT2)

Adenine Nucleotide Translocase-2 (ANT2) is a protein that functions as a mitochondrial transporter for ADP and ATP, playing a key role in cellular metabolism and energy regulation. It is particularly important in cancer cells and highly proliferative tissues, where it can help maintain mitochondrial function and prevent cell death (apoptosis).

High levels of ANT2 expression are linked to cancer. Because of its anti-apoptotic role and ability to support the high energy demands of tumors, it is considered a potential target for cancer therapies.

In aged skin, ANT2 promotes wound healing by influencing metabolic shifts to increase ATP production, inducing cell proliferation, and modulating inflammation.

In adipose tissue, ANT2 activity contributes to intracellular hypoxia and dysfunction. Knockdown of ANT2 can improve insulin sensitivity and glucose tolerance by reducing adipocyte oxygen demand.

ANT2 is being explored as a target for cancer therapy because it is highly expressed in cancer cells and plays a key role in their energy metabolism. By inhibiting ANT2, researchers aim to disrupt the energy supply to cancer cells, leading to cell cycle arrest, apoptosis, and the potential for "supercharging" immune cells like T cells to better fight tumors.

CAR T-cell therapy for blocking ANT2 is a novel approach that involves reprogramming T-cells by blocking the ANT2 protein to improve their energy supply, making them more effective at fighting cancer.
This metabolic reprogramming enhances T-cell anti-tumor immunity by making them more active, resilient, and better at killing cancer cells.
It's a way to "power up" the immune cells before they even leave the lab. (Energy rewiring)

While traditional CAR T-cell therapy targets specific cancer antigens, this strategy focuses on modifying the T-cells' own internal machinery to boost their function.
In this newer strategy, researchers have found that blocking the ANT2 protein within the T-cells themselves changes their metabolism.
While CAR T-cell therapies targeting specific antigens are approved for certain cancers, the ANT2-blocking strategy is still in its early stages of development.

Gene therapy: Researchers are using RNA interference techniques like short hairpin RNAs (shRNA) to specifically target and "knock down" ANT2 expression in cancer cells.
These shRNAs are delivered through methods like viral vectors (e.g., adenovirus) or non-viral methods (like using Polyethylenimine, PEI, with ultrasound)
to effectively reduce ANT2 levels and induce effects such as cell death and tumor regression.
Plasmids encoding shRNAs can be delivered directly into cells through transfection, which can be done using agents like Lipofectamine 2000, as described in National Institutes of Health (NIH).
These shRNAs are designed to specifically bind to the messenger RNA (mRNA) of ANT2, leading to its degradation and preventing the protein from being synthesized.

Combination therapies
Future strategies may involve combining ANT2 inhibition with existing cancer treatments, like immunotherapy or chemotherapy.

Potential challenges
Cancer cells can be metabolically flexible, which may allow them to adapt and evade single-target therapies.

Understanding the specific roles of different ANT isoforms (like ANT1 and ANT2) and their interactions is an ongoing area of research.

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27/11/2025

Immune Check Point Inhibitor Therapy or Anti-The PD-1/PDL-1 Therapy

The PD-1/PD-L1 pathway is a crucial immune checkpoint that acts as a brake on the immune system to prevent autoimmunity and tissue damage. In cancer, tumor cells exploit this pathway by expressing PD-L1 to bind with PD-1 on T-cells, which inhibits the T-cells from recognizing and destroying the cancer cells.
This creates an "immune escape" mechanism for tumors, leading to a weakened anti-tumor immune response.

How the pathway works
Normal function: In a healthy immune response, the PD-1/PD-L1 pathway promotes immune tolerance by preventing excessive inflammation and autoimmune attacks on healthy tissues. PD-L1 is expressed on normal tissue cells and antigen-presenting cells, and when it binds to PD-1 on T-cells, it sends an inhibitory signal that slows down or deactivates the T-cell.
Cancer's exploitation: Many cancer cells overexpress PD-L1, creating a "shield" to evade the immune system.
When PD-L1 on the cancer cell binds to PD-1 on an immune T-cell, it sends a signal that inhibits the T-cell.
This inhibits the T-cell's activation, proliferation, and ability to kill other cells.
It also decreases the production of pro-inflammatory cytokines and promotes the release of immunosuppressive ones, further suppressing the immune response.

Therapeutic application
Immune checkpoint inhibitor therapy: Drugs have been developed to block the interaction between PD-1 and PD-L1.
By blocking this interaction, the "brake" is released, allowing the T-cells to remain active and recognize and attack the cancer cells.
This type of therapy, also known as anti-PD-1/PD-L1 therapy, has shown success in treating various cancers by restoring the immune system's ability to fight the tumor.

Anti-PD-1/PD-L1 therapy is a type of cancer immunotherapy that uses antibodies to block the interaction between PD-1 (on T cells) and PD-L1 (on tumor cells). This blockade "releases the brakes" on the immune system, allowing T cells to recognize and kill cancer cells.
Approved drugs like
(a human IgG4 monoclonal antibody) and (a humanized monoclonal antibody of the IgG4 kappa type)
are used to treat various cancers, and potential side effects include immune-related adverse events (irAEs) affecting organs like the skin, liver, and lungs.

Challenges and future directions
Resistance: A major obstacle is that some patients do not respond to the therapy due to resistance mechanisms.
Predicting response: Researchers are working on biomarkers, such as blood tests, to predict which patients will benefit most from the treatment.
New strategies: Research is also focused on combination therapies and understanding the mechanisms of resistance to improve outcomes.

26/11/2025

Scientists capture stunning real-time images of DNA damage and repair

Scientists have created a live-cell DNA sensor that reveals how damage appears and disappears inside living cells, capturing the entire repair sequence as it unfolds. Instead of freezing cells at different points, researchers can now watch damage flare up, track repair proteins rushing to the site, and see the moment the DNA is restored. Built from a natural protein that binds gently and briefly to damaged DNA, the sensor offers a true-to-life view of the cell’s internal emergency response.

DNA damage mechanisms include endogenous processes like those from metabolism (Reactive oxygen species (ROS), Spontaneous deamination and Replication errors) and
exogenous factors (UV radiation,
Ionizing radiation (X-ray and gamma ray) and Chemicals (Alkylating agents and some toxins)
which cause base modifications, strand breaks, and cross-linking. If unrepaired, this damage can lead to mutations, genomic instability, and cellular dysfunction, with serious effects including cancer, aging, and neurodegenerative diseases.

Cells have sophisticated DNA repair mechanisms to counteract this damage.

Mechanisms of DNA damage
Endogenous damage: Arises from internal cellular processes.
Reactive oxygen species (ROS): Generated during normal metabolism, ROS can cause oxidative damage to bases, like forming 8-oxoguanine.
Spontaneous deamination: Water can hydrolyze the N-glycosyl bonds and cause bases to change, such as cytosine becoming uracil.
Replication errors: Mistakes during DNA replication can lead to mismatched base pairings.

Exogenous damage: Caused by external factors.
UV radiation: Can form dimers between adjacent pyrimidines, like thymine, distorting the DNA helix.
Ionizing radiation: X-rays and gamma rays can cause single- and double-strand breaks.
Chemicals: Alkylating agents can add alkyl groups to DNA bases (forming adducts), and some toxins can cause cross-linking.

Effects of DNA damage
: Unrepaired damage can lead to permanent changes in the DNA sequence, called mutations.
1. Small-scale mutations: Include point mutations where a single base is changed.
2. Large-scale mutations: Can include frameshift mutations or larger alterations.

instability: Accumulation of unrepaired damage can lead to a general instability in the genome.
: A high correlation exists between the accumulation of mutations from DNA damage and the development of cancer.
: In non-replicating cells, unrepaired DNA damage can accumulate and contribute to the aging process.
diseases: High levels of DNA damage are linked to the progression of disorders like Alzheimer's and Parkinson's disease.
death: If damage is extensive, the cell may trigger programmed cell death (apoptosis) to prevent further mutation.

BER Mechanism.
The primary repair process to eliminate DNA damage is the base excision repair pathway, or BER. The BER process is used when DNA is damaged by reactive oxygen species, single-strand breaks, or alkylating agents through oxidation.

Base excision repair (BER):
Step 1: Glycosylase removes the base lesion.
Step 2: AP endonuclease and AP lyase make nicks in the strand. Step
3: DNA polymerase fills the gap.

Mechanism
Damage recognition: A DNA glycosylase detects and removes a single damaged base, such as uracil, 8-hydroxyguanine, or an alkylated base.
AP site formation: This action leaves behind an abasic (AP) site, where the sugar-phosphate backbone is intact but the base is missing.
Incision and removal: An AP endonuclease nicks the DNA backbone at the AP site, removing the sugar-phosphate group from the 5' end.
DNA synthesis: A DNA polymerase fills the gap by adding the correct nucleotide.
Ligation: A DNA ligase seals the remaining nick in the DNA backbone, restoring the intact double helix.

Significance
Prevents mutations: BER is crucial for genome stability and prevents mutations that can arise from base damage.
Maintains health: Its proper function helps protect against diseases like cancer, premature aging, and neurodegeneration.
Location: The process occurs in both the cell's nucleus and mitochondria.

Types of repair
Short-patch BER: The most common pathway, which involves the insertion of a single nucleotide.
Long-patch BER: A less common, alternative pathway used for certain types of lesions, where a longer stretch of nucleotides is synthesized and replaced.

A live-cell DNA sensor that reveals how damage appears and disappears inside living cells.
https://www.sciencedaily.com/releases/2025/11/251123085554.htm

25/11/2025

Metformin and Gerotherapeutic

Metformin lowers blood glucose by reducing hepatic glucose production, decreasing intestinal glucose absorption, and increasing insulin sensitivity in peripheral tissues. It primarily works by activating AMP-activated protein kinase (AMPK), which inhibits gluconeogenesis in the liver, and also reduces the absorption of glucose from the intestines. This leads to lower blood glucose levels without typically causing hypoglycemia or weight gain.

Key mechanisms of action
Reduces liver glucose production: Metformin inhibits gluconeogenesis (the liver's production of glucose) through several pathways, including the activation of AMPK.

Increases insulin sensitivity: It improves the body's response to insulin, leading to increased glucose uptake and utilization by muscles and other tissues.
Decreases intestinal glucose absorption: Metformin can decrease the amount of glucose absorbed from the food you eat.

Inhibits mitochondrial function: Its effects are linked to the inhibition of mitochondrial complex I, which can lead to a decrease in cellular energy and activation of AMPK.
Activation of AMPK may have a role in extending lifespan, as seen in studies of caloric restriction and aging in model organisms.

Modulates gut microbiome: Recent research suggests metformin alters the gut microbiome, which may contribute to its therapeutic effects.

Side effects are common, with gastrointestinal problems such as nausea, diarrhea, loss of appetite and abdominal discomfort, occurring in up to 75% of those who take metformin.

Metformin, however, can cause lactic acidosis in conditions where lactic acid production is high and the disposal of lactic acid is reduced. In conditions such as circulatory failure, sepsis, and anoxia or hypoxia, metformin use may result in lactic acidosis and should be avoided. While uncommon, metformin can also cause blood glucose to drop too low and lactic acidosis.
Metformin may have an adverse effect on renal function in patients with type 2 DM and moderate CKD.
It can also cause fatigue, weight loss, and low vitamin B12 levels.

Slow brain aging and longevity
A recent study suggests it works directly in the brain, which could lead to new types of treatment.
In their 2025 study, tests on mice showed metformin traveling to the VMH, where it helps tackle type 2 diabetes by essentially turning off Rap1.
When the researchers bred mice without Rap1, metformin then had no impact on a diabetes-like condition – even though other drugs did.
It's strong evidence that metformin works in the brain, through a different mechanism than other drugs.
It very probably works through the brain, as well as the liver and the gut.
In addition, metformin is known for other health benefits, such as slowing brain aging and improve lifespan.

Metformin is also considered a gerotherapeutic: a drug able to slow down various aging processes in the body. For example, it's been shown to limit DNA damage and promote gene activity associated with long life.

The study's key finding is that the use of metformin is associated with a 30% lower risk of death before age 90 compared to use of sulfonylurea.

Metformin has been prescribed to people with type 2 diabetes to manage blood sugar for more than 60 years, but scientists haven't been exactly sure how it works.

25/11/2025

Amyotrophic lateral sclerosis, causes, symptoms, treatment, stem cell therapy
Rehabilitation and using of injection B12 for muscle stiffness and pain.

Amyotrophic lateral sclerosis, also known as motor neuron disease or—in the United States and Canada—Lou Gehrig's disease, is a rare, terminal neurodegenerative disorder that results in the progressive loss of both upper and lower motor neurons that normally control voluntary muscle contraction. Wikipedia

The exact cause of ALS is unknown, but it is believed to result from a combination of genetic and environmental factors. While most cases are sporadic (no clear cause), about 5–10% are familial, meaning they are inherited through a specific gene mutation. Risk factors include genetic mutations (especially in the C9orf72 and SOD1 genes), age, s*x, military service, smoking, and exposure to environmental toxins like heavy metals and pesticides.

Early symptoms of ALS include muscle twitches, cramps, and stiffness, often starting in a limb. As the disease progresses, it causes increasing muscle weakness, which can lead to slurred speech, difficulty swallowing, and eventually, problems with breathing.
Other symptoms may include tripping and falling, muscle wasting, difficulty using arms and legs, leading to paralysis and
uncontrolled crying or laughing in late-stage ALS.

Treatmens
Medications
Riluzole (Rilutek, Tiglutik, Exservan): An oral medication that may prolong survival by several months by blocking the release of the neurotransmitter glutamate.
Edaravone (Radicava): An IV or oral suspension that can slow the decline in physical function.
Tofersen (Qalsody): A gene-based therapy that can help reduce damage in patients with a specific SOD1 genetic mutation.

Symptom-management medications: Other drugs are available to help with symptoms like muscle cramps, stiffness, and excess saliva.

Stem call theraoy
The most common approach involves mesenchymal stem cells (MSCs) that can release growth factors to support neuron health or modulate the immune system to reduce inflammation. While early trials have shown some potential for slowing functional decline, more research is needed, and results have not been consistently positive enough for approval.

Stem cell therapy for ALS is only available through clinical trials. It is crucial to discuss this option with your doctor, who can help find potential trials and evaluate eligibility.

Rehabilitation
Rehabilitation for Amyotrophic Lateral Sclerosis (ALS) is a multidisciplinary approach including physical, occupational, speech, and respiratory therapy to help patients maximize function, maintain independence, and improve quality of life. Therapies focus on managing symptoms like muscle stiffness and cramps, preventing falls, adapting daily activities, assisting with communication and swallowing, and maintaining respiratory strength. While there is no cure for ALS, rehabilitation helps patients manage the disease and live more fulfilling lives.

Multiple vitamin B12 injection near the nerve and body sites that improves muscle improves and relieves muscle stiffness and pain.
Range-of-motion and stretching exercises should be done to prevent stiffness, muscle cramps, and joint pain.
Both cause induction of neuroplasticity but structural and functional synaptic pasticity may be not adequate for progressive destruction of nerve in ALS.

Adequate modulation of structural and functional synaptic plasticity may likely support function sparing and delay disease progression.

Structural and functional synaptic alterations and plasticity may occur at all levels of the central and peripheral nervous systems and at all stages of ALS disease. Despite evidence showing that certain cell populations are more vulnerable to cell stress and degeneration, it remains unclear which of these cell types will degenerate first.

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