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|| Pharmacology || New Study Finds Metformin’s Extended Reach to Offer a Treatment Option for Neuro-developmental Disorder Periventricular Heterotopia ||


|| Sunday: September 24: 2023 || ά. An international research team has shed light on the underlying mechanisms of a brain abnormality, Periventricular Heterotopia:PH, that occurs during human foetal development. By uncovering these hidden mechanisms, scientists could, potentially, design new strategies to better understand and, may, find new therapeutics to treat the condition.

PH is a neuro-developmental condition, that’s characterised by an abnormal migration of neuronal cells. These cells end up clustering around ventricles, the cavities of the brain. The disorder becomes apparent with recurrent seizures. It is genetically heterogenous, meaning that mutations in distinct genes may lead to PH. The collaborative research team, led by the University of Ottawa’s Dr Armen Saghatelyan, aimed to uncover the migratory mechanisms of grafted human neuronal progenitor cells, derived from PH patients in the brains of an immune-deficient mouse model. ::::ω::::

|| Readmore at || || 240923 ||





|| Prospect For A Cure For Common Leukaemia Appears Close ||


|| Friday: September 22: 2023 || ά. A ground-breaking chronic myeloid leukaemia:CML test can help identify patients, who are strong candidates for life-long treatment free remission:TFR, meaning they are effectively cured of the disease. Research into CML has made life-saving discoveries over the past few decades. In the early 1990s, the disease brought an average survival rate of less than five years.

The development of tyrosine kinases inhibitors:TKIs as a treatment dramatically increased survival rates but, for many patients, caused debilitating side effects while losing efficacy over time. Ensuing decades of diligent research saw next-generation TKIs developed to deliver longer-lasting impact and less side effects but, still patients faced lifelong management of the disease.

Dr Ilaria Pagani, the First Author on the research paper, which has just been published in the journal Blood, says that this break-through in chronic myeloid leukaemia:CML research is the cumulation of six years of investigation.  “With this discovery, we move the conversation for people with CML from one of life-long disease control to one of cure.” She said. “With the test we have developed, we can predict with a high degree of accuracy, who will have an excellent probability of on-going TFR.”

By 2006, work led by Dr Pagani’s Adelaide-based colleagues Professor David Ross and Professor Tim Hughes, in collaboration with international research teams, showed that it was possible for patients, who had excellent responses to treatment to, simply, stop taking their medication and remain in remission. For those people, who could sustain it, TFR is effectively a cure but, there was still no way to tell, who would be successful and who would relapse and need to restart therapy.

These findings are significant because they challenge an existing assumption that response to TKI therapy is best assessed by measuring the presence of the leukaemia-defining BCR::ABL1 fusion gene in the blood of a CML patient. “Until now, the assumption was that every blood cell, that contained BCR::ABL1 was evidence of persistent disease, that could lead to relapse.” Dr Pagani said.

“What we have now shown is that the chances of relapse depend greatly on which type of cell the disease is detected in, if, it’s in what are known as myeloid cells, then the chances of TFR are sadly pretty low but, if, it’s in lymphocytes then that has limited impact on relapse likelihood.”

This research involved a broad collaboration between Dr Pagani’s SAHMRI-based team, the University of Adelaide, the University of South Australia, Flinders University, SA Health and Perth-based researchers. It has been funded in part by the Leukaemia Foundation and the Cancer Council SA Beat Cancer Project.

The material outcome of this work is a blood test, that more accurately determines the best course of treatment, giving TFR candidates greater confidence before ceasing treatment. “This new lineage-specific BCR:ABL1 test can now be used to determine who can safely stop therapy, who should continue therapy for a longer period, and who needs a different therapy before they could be considered for TFR.” Dr Pagani said.

“Sadly, not everyone will be a candidate for TFR with current approaches but, for those whose chance of relapse is high, we will now have greater information with which to design new therapeutic approaches, that can lead to TFR, even, for these more challenging patients.

"Ultimately, our aim is to design a curative approach for all CML patients so that TFR becomes the mainstream pathway, rather than a pathway followed by a lucky minority."

CML is a relatively rare leukaemia in terms of diagnosis but, the success of researchers and clinicians to improve survival rates mean that it is an increasingly common for people to be living with the condition. CML causes the bone marrow to produce too many white blood cells, which can adversely affect normal blood cell production. In time, a shortage of blood cells can present as infection, anaemia or unexplained bleeding or bruising. People with CML might, also, experience discomfort beneath their ribs on the left-hand side of their body due to an enlarged spleen. || ΕΛ ||  

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|| New Study on the Development of Alzheimer’s Disease Finds a Possible Cause of Inflammation ||


|| Wednesday: August 30: 2023 || ά. Alzheimer’s Disease is characterised by the accumulation of plaques of the amyloid-β protein, chronic inflammation and impaired neuronal function in the brain. The most significant genetic risk factor for the disease is the protein, apoE4, a variant of apolipoprotein E, which is known for, among other things, advancing the onset of the Alzheimer’s.

Alzheimer’s Disease is a slowly progressing memory disorder with more than 10 million new cases every year. As the population ages, the number of patients with the disease will rise considerably. In the future, Alzheimer’s Eisease will increase human suffering, as well as, the burden on public health and the economy. While more than half of all individuals with Alzheimer’s Disease carry this variant, the exact effect of apoE4 on the development of the disease has remained unknown.

A new Study, recently completed at the University of Helsinki identified a more accurate link between the apoE4 gene and the part of the human immune system, that underlies Alzheimer’s. This is known as the complement system and it contributes to the destruction of foreign cells and easily triggers inflammatory responses in the body.

“We found that apoE4 poorly binds factor H, a regulatory factor of immunity. The factor H molecule is crucial in preventing complement-mediated inflammation.” says Karita Haapasalo, the Principal Investigator of the Study leading the Inflammation and Infections research group at the University of Helsinki.

“Usually, apoE binds factor H to the amyloid-β aggregates in the brain, thus, reducing local inflammation. But apoE4 does not.” She points out. This results in the accumulation of harmful amyloid-β aggregates and inflammation in the brain. Binding factor H to apoE4 could present a potential solution to preventing changes in the brain, that lead to the onset of Alzheimer’s. Further research will soon be conducted to look for such a bridging molecule.

The amyloid-β aggregates, associated with Alzheimer’s Disease begin to form in the brain decades before the diagnosis of the memory disorder. Since the mechanism, underlying these changes has not been sufficiently well known, drug development has focused on stopping or slowing down changes, that have already taken place. “The drugs currently in use do not prevent the onset of the disease itself.” Says Haapasalo.

“Determining the molecular mechanisms, that affect the onset of Alzheimer’s is important for developing curative drugs and therapies in the future.”

The study, published in May in the EMBO Reports journal, was carried out both by using experimental cell culture models and investigating brain biopsy samples from patients with idiopathic normal pressure hydrocephalus:iNPH syndrome, in co-operation with the University of Eastern Finland, Kuopio University Hospital and international research organisations.

Original Article: Reduced binding of apoE4 to complement factor H promotes amyloid-β oligomerization and neuroinflammation: Larisa Chernyaeva, Giorgio Ratti, Laura Teirilä, Satoshi Fudo, Uni Rankka, Anssi Pelkonen, Paula Korhonen, Katarzyna Leskinen, Salla Keskitalo, Kari Salokas, Christina Gkolfinopoulou, Katrina E Crompton, Matti Javanainen, Lotta Happonen, Markku Varjosalo, Tarja Malm, Ville Leinonen, Angeliki Chroni, Päivi Saavalainen, Seppo Meri, Tommi Kajander, Adam JM Wollman, Eija Nissilä, Karita Haapasalo: EMBO:

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