Post by Admin on May 13, 2022 17:18:22 GMT
Could a certain level of stress help reverse dementia?
www.medicalnewstoday.com/articles/could-a-certain-level-of-stress-help-reverse-dementia
Researchers investigated whether stressing certain parts of cells leads to the misfolding of proteins characteristic of neurodegenerative conditions such as dementia.
They found that rather than increasing misfolding, certain amounts of stress can cause protein aggregates to unfold.
The researchers hope that their findings may one day provide a basis for new treatments for neurodegenerative conditions.
A common characteristic of neurodegenerative conditions, such as Alzheimer’s and Parkinson’s, is a buildup of misfolded proteinsTrusted Source such as beta-amyloid and tau.
To avoid this buildup, healthy cells have in-built processesTrusted Source that monitor protein folding to ensure that proteins are correctly folded and any misfolded proteins are destroyed. Errors in these processes may resultTrusted Source in neurodegenerative conditions.
In a recent study, researchers discovered that the systolic heat shock protein Hsp70 chaperoneTrusted Source and its assisting system had the ability to resolve protein buildups in the cell’s cytoplasm, the material within a cell excluding the nucleus.
Knowing whether a similar ability exists in the Endoplasmic Reticulum (ER)—a site in the cell that manufactures around a third of cellular proteins—could improve researchers’ understanding of neurodegeneration pathology.
In a recent study, researchers hypothesized that ‘adding stress’ to the ER would lead to protein misfolding and, eventually, buildups. They found, however, that the opposite was true.
“This work showed that stressing cells grown in a dish with chemicals can help clear abnormal clumps of proteins from a structure inside the cells called endoplasmic reticulum,” Professor Tara Spires-Jones, deputy director of the Centre for Discovery Brain Sciences at the University of Edinburgh, who was not involved in the study, told Medical News Today.
“The stress caused activation of a chaperone or ‘helper’ protein which can help other proteins refold into their normal shapes instead of toxic clumps,” she added.
The study was published in NatureTrusted Source.
Sodium selenate: A potential future treatment for early-onset dementia
www.medicalnewstoday.com/articles/sodium-selenate-a-potential-future-treatment-for-early-onset-dementia
Researchers assessed the safety and tolerability of sodium selenate when treating dementia.
They found that sodium selenate is safe and well-tolerated by patients.
They now plan to conduct a larger, placebo-controlled trial.
Behavioral variant frontotemporal dementia (bvFTD) is the second most commonTrusted Source form of dementia in younger patients and can occur as early as age 45.
Around 45% of bvFTD cases are caused by excessive tau protein in the brain, which interferes with neuronal structure and leads to neurodegeneration.
The levels and activity of an enzyme called phosphatase 2 (PP2A) are linked to reduced levels of neurodegeneration. Stabilizing and upregulating this enzyme may thus help reduce tau build-ups.
Sodium selenate has been shown to upregulate PP2A activity and reduce tau levels in animal models of dementia and mild-moderate Alzheimer’s disease.
Knowing whether these findings may be replicated in humans could pave the way for new treatment options.
Recently, researchers conducted a Phase 1b trial to understand the safety and tolerability profile of sodium selenate in patients with bvFTD.
The researchers found that sodium selenate is safe and well-tolerated in patients with bvFTD, and that further study is now warranted to investigate the drug.
The study was published in the Alzheimer’s Association’s journal Translational Research and Clinical InterventionsTrusted Source.
Phase 1b trial
For the study, the researchers enrolled 12 participants with bvFTD with a median age of 61 years old. Each received 10 mg of sodium selenate three times a day, at week 4 they started receiving 15 mg of sodium selenate which was maintained for 52 weeks.
Patients underwent clinical visits at baseline, during treatment, and four weeks after completion.
Clinical measures included MRI scans at baseline and at week 52 to calculate brain volume change, alongside blood and cerebrospinal fluid samples to verify changes in neurodegenerative markers.
The patients also filled in various questionnaires to track cognitive, emotional, and behavioral measures.
In the end, the researchers found that sodium selenate was safe and well-tolerated by patients with bvFTD.
While patients experienced no serious adverse events, all experienced at least one adverse effect, the most common of these being alopecia and nail disorders.
Beyond safety and tolerability, the researchers noted that patients underwent a small decline in cognition and behavior over the study period. They also experienced no change in tau levels following treatment.
While a small number of participants showed a substantial loss in brain volume, most experienced relatively slow brain atrophy rates.
www.medicalnewstoday.com/articles/could-a-certain-level-of-stress-help-reverse-dementia
Researchers investigated whether stressing certain parts of cells leads to the misfolding of proteins characteristic of neurodegenerative conditions such as dementia.
They found that rather than increasing misfolding, certain amounts of stress can cause protein aggregates to unfold.
The researchers hope that their findings may one day provide a basis for new treatments for neurodegenerative conditions.
A common characteristic of neurodegenerative conditions, such as Alzheimer’s and Parkinson’s, is a buildup of misfolded proteinsTrusted Source such as beta-amyloid and tau.
To avoid this buildup, healthy cells have in-built processesTrusted Source that monitor protein folding to ensure that proteins are correctly folded and any misfolded proteins are destroyed. Errors in these processes may resultTrusted Source in neurodegenerative conditions.
In a recent study, researchers discovered that the systolic heat shock protein Hsp70 chaperoneTrusted Source and its assisting system had the ability to resolve protein buildups in the cell’s cytoplasm, the material within a cell excluding the nucleus.
Knowing whether a similar ability exists in the Endoplasmic Reticulum (ER)—a site in the cell that manufactures around a third of cellular proteins—could improve researchers’ understanding of neurodegeneration pathology.
In a recent study, researchers hypothesized that ‘adding stress’ to the ER would lead to protein misfolding and, eventually, buildups. They found, however, that the opposite was true.
“This work showed that stressing cells grown in a dish with chemicals can help clear abnormal clumps of proteins from a structure inside the cells called endoplasmic reticulum,” Professor Tara Spires-Jones, deputy director of the Centre for Discovery Brain Sciences at the University of Edinburgh, who was not involved in the study, told Medical News Today.
“The stress caused activation of a chaperone or ‘helper’ protein which can help other proteins refold into their normal shapes instead of toxic clumps,” she added.
The study was published in NatureTrusted Source.
Sodium selenate: A potential future treatment for early-onset dementia
www.medicalnewstoday.com/articles/sodium-selenate-a-potential-future-treatment-for-early-onset-dementia
Researchers assessed the safety and tolerability of sodium selenate when treating dementia.
They found that sodium selenate is safe and well-tolerated by patients.
They now plan to conduct a larger, placebo-controlled trial.
Behavioral variant frontotemporal dementia (bvFTD) is the second most commonTrusted Source form of dementia in younger patients and can occur as early as age 45.
Around 45% of bvFTD cases are caused by excessive tau protein in the brain, which interferes with neuronal structure and leads to neurodegeneration.
The levels and activity of an enzyme called phosphatase 2 (PP2A) are linked to reduced levels of neurodegeneration. Stabilizing and upregulating this enzyme may thus help reduce tau build-ups.
Sodium selenate has been shown to upregulate PP2A activity and reduce tau levels in animal models of dementia and mild-moderate Alzheimer’s disease.
Knowing whether these findings may be replicated in humans could pave the way for new treatment options.
Recently, researchers conducted a Phase 1b trial to understand the safety and tolerability profile of sodium selenate in patients with bvFTD.
The researchers found that sodium selenate is safe and well-tolerated in patients with bvFTD, and that further study is now warranted to investigate the drug.
The study was published in the Alzheimer’s Association’s journal Translational Research and Clinical InterventionsTrusted Source.
Phase 1b trial
For the study, the researchers enrolled 12 participants with bvFTD with a median age of 61 years old. Each received 10 mg of sodium selenate three times a day, at week 4 they started receiving 15 mg of sodium selenate which was maintained for 52 weeks.
Patients underwent clinical visits at baseline, during treatment, and four weeks after completion.
Clinical measures included MRI scans at baseline and at week 52 to calculate brain volume change, alongside blood and cerebrospinal fluid samples to verify changes in neurodegenerative markers.
The patients also filled in various questionnaires to track cognitive, emotional, and behavioral measures.
In the end, the researchers found that sodium selenate was safe and well-tolerated by patients with bvFTD.
While patients experienced no serious adverse events, all experienced at least one adverse effect, the most common of these being alopecia and nail disorders.
Beyond safety and tolerability, the researchers noted that patients underwent a small decline in cognition and behavior over the study period. They also experienced no change in tau levels following treatment.
While a small number of participants showed a substantial loss in brain volume, most experienced relatively slow brain atrophy rates.