Estrogen-only menopausal hormone therapy linked to fewer Alzheimer’s hallmarks in women

Good news!

Notice how Stanford University strenuously avoids to mention women in the first article below even though this health subject is about women!!! A typical case of deplorable ideology and indoctrination? It is certainly very strange!

"In brief

• Stanford Medicine researchers examined autopsied brains for Alzheimer’s defining pathological hallmarks to learn how menopausal hormone therapy relates to the disease.
• The study found that estrogen-only therapy was associated with fewer of these Alzheimer’s hallmarks and better performance on memory tests and in the ability to function independently.
• The finding challenges a longstanding recommendation against hormone therapy for memory decline and points to a possible benefit against dementia for women who reach menopausal age without a uterus.

...

The study ... is the first to measure the connection between menopausal hormone therapy, or MHT, and reductions in Alzheimer’s-related pathological deposits in autopsied brains. ..."

From the abstract:

"Background and Objectives

Although evidence suggests that the neurophysiologic impact of estrogen decline during menopause may contribute to increased risk of Alzheimer disease (AD) in women, the effect of menopausal hormonal therapy (MHT) on AD risk requires further study. We sought to examine the associations between MHT use and neuropathologic, clinical, and imaging/fluid biomarker outcomes.

Methods

In this cohort study, we tested the association between estrogen-only MHT use and dementia outcomes in female participants using 2 independent, large-scale data sets:

National Alzheimer's Coordinating Center (NACC) and

Alzheimer's Disease Neuroimaging Initiative (ADNI).

Participants included women 50 years and older with self-reported use of estrogen-only MHT or no self-reported use of MHT. Clinical, imaging/fluid biomarker, and neuropathologic outcomes were examined. Research was performed at academic medical centers.

Results

Neuropathologic data were collected from
NACC for 258 MHT users (mean age of death = 81.9, SD = 19.5) and 2,701 non-MHT users (mean age of death = 82.2, SD = 11.0).

The ADNI cohort included 110 MHT users (mean age = 76.5, SD = 7.5) and 1,948 non-MHT users (mean age = 73.2, SD = 8.9).

The odds of increased AD pathology on autopsy (primary outcome) were significantly decreased in MHT users relative to nonusers (odds ratio [OR] 0.65, 95% CI 0.48–0.88, p = 0.005).

MHT use was associated with secondary outcomes including significantly decreased amyloid pathologic load assessed through plasma (β = 0.44, 95% CI 0.16–0.73, p = 0.0025) and CSF (β = 0.07, 95% CI 0.002–0.13, p = 0.030).

MHT use was associated with significantly lower odds of clinical dementia diagnoses (OR 0.61, 95% CI 0.55–0.67, p < 0.0001) and lower odds of symptoms of memory/functional decline (OR 0.67, 95% CI 0.61–0.74, p < 0.0001).

Discussion

Our findings demonstrate small but significant associations between MHT use during later life and a range of AD-related neuropathologic and clinical outcomes in 2 large cohorts of female participants.

Although our results do not address causality and have limited generalizability due to the retrospective nature of the study, they suggest a protective effect of MHT use in the dementia course."

Estrogen-only therapy linked to fewer Alzheimer’s hallmarks | Stanford Report "Some studies have reported that estrogen-only menopausal hormone therapy raises dementia risk. New research on Alzheimer’s disease hallmarks in autopsied brains indicates the opposite."

Study ties estrogen-based menopausal hormone therapy to lower Alzheimer’s risk "Some studies have reported that menopausal hormone therapy raises dementia risk. A new study that analyzed Alzheimer’s-disease hallmarks in autopsied brains indicates the opposite."

Association Between Menopausal Hormone Therapy and Alzheimer Disease Neuropathology (no public access)

Average testosterone levels in men declined by 54% between 1972 and 2019 according to an international study of over 118,000 men

Serious stuff, if confirmed! Of course, climate change needed to be implicated by The Guardian!

Unfortunately, I was not able to find the study e.g. via Google search, Google Scholar, the Hebrew University-Hadassah Braun School of Public Health and Community Medicine etc. Presumably, this study has not yet been published.

"Average testosterone levels in men declined by 54% between 1972 and 2019, according to data presented this week at the annual meeting of the European Society of Human Reproduction and Embryology in London; researchers say rising obesity and diabetes are the key drivers but also highlighted endocrine-disrupting chemicals and climate change as potential factors [???]. ..."

"... These findings come from an international study led by Prof. Hagai Levine of the Hebrew University-Hadassah Braun School of Public Health and Community Medicine. ..." (Google search)

Global Health NOW: Pandemic-Era Push for PPE Stalls; and Long Road of Autism Advocacy in Guinea

Mammalian mothers and their babies need the oxytocin love hormone

Amazing stuff!

Notice again the gender bias and misandry here: The researchers apparently did not bother to investigate the male mouse/father. Is the father so irrelevant here?

"... Oxytocin has been shown to play a part in forming social bonds, including for mothers during grooming and nursing. To test the hormone’s role in babies, researchers separated 15-day-old mouse pups from their mothers for 3 hours. When they were reunited, the researchers measured ultrasonic vocalizations, noises that baby mice make to signal distress and catch their mothers’ attention. The team also used invasive and noninvasive methods to simultaneously measure the activity of oxytocin-producing neurons in the mice’s brains.

Indeed, vocalizations and oxytocin production increased upon the familial reunions, declining as the mother comforted the baby. But when mouse pups were reunited with an anaesthetized mama, their vocalizations stayed high. The researchers hypothesize that synchronized oxytocin release by the mothers and babies upon reunion helps regulate their emotions and strengthen social relationships. ..."

From the abstract of the Perspective:

"Abstract

For most mammals, social bonding between mothers and infants is a fundamental, evolutionarily conserved behavior that is crucial for offspring survival, emotional regulation, and the acquisition of social skills necessary for future interactions. Early-life experiences, especially maternal care, shape developmental trajectories, profoundly influencing cognitive, emotional, and social competencies into adulthood. In rodents, the neuropeptide oxytocin has been widely recognized for its central role in maternal behaviors toward infants such as nesting, grooming, and nursing.

Yet comparatively little is known about how oxytocin regulates infant behaviors toward mothers, particularly during episodes of maternal separation and reunion. ... Zelmanoff et al. report real-time changes in the activity of oxytocin-producing neurons in mouse pups during maternal separation and reunion, offering insights into how offspring actively contribute to maternal-infant bonding."

From the editor's summary and abstract:

"Editor’s summary

The neuropeptide oxytocin has been shown to play a major role in driving parental behavior. However, its role in early life remains to be fully elucidated. Zelmanoff et al. investigated the role of oxytocin in modulating social behavior in mouse pups during separation and reunion with their mothers ... Pups separated from their mothers produced more ultrasonic vocalizations upon reunion, and the effect was modulated by the activity of oxytocin-expressing neurons. Pharmacological and optogenetic inhibition of these neurons attenuated ultrasonic vocalizations, suggesting that oxytocin plays a major role in determining social behavior during development. ...

Structured Abstract

INTRODUCTION

Oxytocin is a brain hormone that plays a critical role in regulating social behavior. Although much research has focused on how oxytocin supports adult behaviors such as pair-bonding and caregiving, far less is known about how this system functions during early life. The early postnatal period is a time of critical social interactions between infants and caregivers, and disruptions during this period may contribute to developmental disorders. Notably, expression of the oxytocin receptor peaks during infancy in both humans and mice, suggesting that this period represents a critical window of heightened sensitivity to oxytocin signaling. However, technical challenges have limited the study of the oxytocin system during this sensitive time of brain development. As a result, the role of oxytocin in shaping social behavior during infancy remains poorly understood.

RATIONALE

We set out to investigate how oxytocin influences pup behavior during a brief separation from the mother and littermates and subsequent reunion. We focused on vocal communication, as rodent pups emit ultrasonic vocalizations that signal distress but may also reflect social motivation and need. We combined detailed behavioral analysis with fiber photometry, pharmacological intervention, and a novel optogenetic strategy built on wireless silencing of oxytocin neurons in freely behaving pups—a technical advance that overcomes prior limitations in studying brain circuits during early life.

RESULTS

Pups that were acutely separated from their mother and littermates displayed a substantial increase in vocalizations upon reunion, especially when in close proximity to their mother. The rate and type of vocalizations were modulated by nipple attachment behavior. We found that hypothalamic oxytocin neurons increased their activity upon separation, and that this activity was tightly linked with the emission of vocalizations. 

Blocking the oxytocin receptor in pups during separation reduced nipple attachment and altered the pattern of vocal behavior both during separation and reunion.

For increased temporal precision, we developed a new optogenetic method using a highly light-sensitive, red-shifted inhibitory opsin (eOPN3). This allowed us to wirelessly silence oxytocin neurons in untethered pups.

We found that silencing oxytocin neurons during separation disrupted vocal—but not nonvocal—behavior during both the separation and reunion.

CONCLUSION

Our findings reveal a specific role for oxytocin in shaping maternally directed behavior during infancy. We also introduce a noninvasive optogenetic approach for studying brain circuits in developing animals, opening new opportunities to investigate the neural mechanisms underlying early life social behavior. Our work emphasizes the need to gain a more nuanced understanding of oxytocin function and provides a technical platform for studying the social brain during its most formative stages."

ScienceAdviser

Cries into ties (Perspective, no public access) "Oxytocin neurons in mouse pups regulate vocalization to maintain maternal bonds"

Oxytocin signaling regulates maternally directed behavior during early life (no public access)

Oxytocin signaling regulates maternally-directed behavior during early life (preprint, open access)

Graphical abstract

Figure 1:

Acute maternal separation increases maternally-directed behavior upon reunion.

Discovery of role of gut hormone in chronic diarrhoea could aid development of new tests and treatments

Good news!

"However, around one person in every 100 is affected by a condition known as bile acid diarrhoea (also known as bile acid malabsorption), whereby the bile acid is not properly re-absorbed and makes its way into the large intestine (colon). It can trigger urgent and watery diarrhoea, and patients can risk episodes of incontinence.

Bile acid diarrhoea can be difficult to diagnose as there are currently no routine clinical blood tests. Many individuals are given a diagnosis of irritable bowel syndrome (IBS), an umbrella term for a range of conditions. As many as one in 20 people is thought to have IBS, of which an estimated one in three patients with diarrhoea as their main symptom have undiagnosed bile acid diarrhoea.

Studies in mice have previously suggested that the gut hormone known as Insulin-Like Peptide 5 (INSL5) – present in cells at the far end of the colon and rectum – may play a role in chronic diarrhoea. INSL5 is released by these cells when irritated by bile acid.

Researchers ... have been exploring whether this hormone might also underlie chronic diarrhoea in humans. This has been possible thanks to a new antibody test  ... which allows them to measure tiny amounts of INSL5.

A study ... looking at ways to trigger release of the gut hormone GLP-1 – the hormone upon which weight-loss drugs are based – previously found that giving a bile acid enema to healthy volunteers triggered release of GLP-1, but had the unintended consequence of causing diarrhoea. When the ... team analysed samples from this study, they found that the bile acid enema caused levels of INSL5 to shoot up temporarily – and the higher the INSL5 levels, the faster the volunteers needed to use the toilet. This confirmed that INSL5 is likely to play a role in chronic cases of diarrhoea.

When the team analysed samples ... which include samples from patients with bile acid diarrhoea, they found that while levels of INSL5 were almost undetectable in healthy volunteers, they were much higher in patients with bile acid diarrhoea. In addition, the higher the INSL5 level, the more watery their stool samples. ..."

From the abstract:

"Background

Insulin-like peptide 5 (INSL5) is an enteroendocrine hormone expressed in distal colonic ‘L cells’. Bile acid receptor agonists are known to stimulate INSL5 secretion in primary cell culture, and administration of an INSL5 analogue in animals promotes colonic motility.

Objective

This study used a new immunoassay to measure INSL5 in human blood samples, enabling assessment of whether rectal bile acids stimulate INSL5 release in humans and whether INSL5 levels are altered in patients with chronic diarrhoea.

Design

Serum/plasma samples from previously performed studies were used, including healthy volunteers (n=7) who received a rectal enema of taurocholic acid (TCA); fasting and post prandial samples from healthy volunteers (n=10); patients with bile acid diarrhoea (BAD) (n=19) or irritable bowel syndrome with diarrhoea (IBS-D) (n=8); and patients with IBS-D (n=64) treated with ondansetron or placebo.

Results

Rectal TCA but not a control enema promptly elevated plasma INSL5, with the increase in INSL5 correlating negatively with time to, and positively with desire to, defecate post enema.

Healthy volunteers had low INSL5 levels (<100 pg/mL), with no change following a mixed meal.

Patients with BAD had elevated INSL5 levels, with average stool consistency being positively correlated with serum INSL5 (p<0.001). In people with IBS-D, INSL5 was elevated (>100 pg/mL) in 42%, and this subgroup showed greater improvements in stool consistency with ondansetron therapy (p<0.05).

Conclusion

The study highlights that rectal bile acids stimulate INSL5 secretion in humans, and that INSL5 levels are associated with a colonic pro-motility response and pathophysiology of chronic diarrhoea."

Discovery of role of gut hormone in chronic diarrhoea could aid development of new tests and treatments | University of Cambridge "High levels of a hormone found in cells in the gut could underlie many cases of chronic diarrhoea and help explain up to 40% of cases of patients with irritable bowel syndrome with diarrhoea ..."

Insulin-like peptide 5 is released in response to bile acid in the rectum and is associated with diarrhoea severity in patients with bile acid diarrhoea (open access)

FGF21 is a hormone having a variety of beneficial metabolic effects in older mice

Good news! In the future, maybe more hormones, less vitamins & minerals?

"Fibroblast growth factor 21 (FGF21) is a hormone that is primarily produced in the liver, as well as in adipocytes and some other tissues. It has been reported to have a variety of beneficial metabolic effects, but there has been no clear mechanistic explanation for them.

Using mouse models of adipocyte-specific overexpression of FGF21, Gliniak et al. demonstrated that these animals are protected from obesity and live longer overall without losing lean tissue mass or bone mineral density. These beneficial effects of FGF21 were due to a variety of effects on different tissues and organs, including increased energy expenditure, improved insulin sensitivity, and decreased adipose tissue ceramide buildup and inflammation, all of which help to explain the health benefits attributed to this hormone."

From the highlights and abstract:

"Highlights

• FGF21 overexpression in the adult mouse increases survival that is not linked to trade-offs in organismal growth

• FGF21 overexpression prevents obesity, liver steatosis, and loss of lean mass in gerobese mice fed a HFD

• Elevated FGF21 increases energy expenditure but does not affect cold tolerance in mice fed a HFD

• FGF21 reduces ceramide levels in visceral adipose tissue by adiponectin-independent mechanisms

Summary

Approximately 35% of US adults over 65 are obese, highlighting the need for therapies targeting age-related metabolic issues.

Fibroblast growth factor 21 (FGF21), a hormone mainly produced by the liver, improves metabolism and extends lifespan.

To explore its effects without developmental confounders, we generated mice with adipocyte-specific FGF21 overexpression beginning in adulthood. When fed a high-fat diet, these mice lived up to 3.3 years, resisted weight gain, improved insulin sensitivity, and showed reduced liver steatosis.

Aged transgenic mice also displayed lower levels of inflammatory immune cells and lipotoxic ceramides in visceral adipose tissue, benefits that occurred even in the absence of adiponectin, a hormone known to regulate ceramide breakdown.

These results suggest that fat tissue is a central site for FGF21’s beneficial effects and point to its potential for treating metabolic syndrome and age-related diseases by promoting a healthier metabolic profile under dietary stress and extending healthspan and lifespan."

In Other Journals | Science

FGF21 promotes longevity in diet-induced obesity through metabolic benefits independent of growth suppression (open access)

Graphical abstract

How psychological stress increases the risk of bacterial skin infection via defective responses

Amazing stuff!

"... Now, new experiments in mice have revealed that stress makes it harder for certain skin cells to fight off bacteria—leaving the animals vulnerable to more severe infection with Staphylococcus aureus.

To induce stress, scientists confined the mice inside small tubes for three hours a day on three consecutive days, exposing them to S. aureus upon release. The restrained rodents produced more adrenaline, leading to higher levels of a stress-related protein called TGFβ. This protein interferes with specialized skin cells known as dermal fibroblasts and prevents them from making cathelicidin—an antimicrobial molecule that normally plays a key role in the skin’s defense system. As a result, the restrained mice ended up experiencing more severe infections, characterized by larger lesions. Blocking adrenaline or TGFβ, meanwhile, allowed the animals’ skin cells to mount a stronger defense against the bacteria."

From the editor's summary and abstract:

"Editor’s summary

Psychological stress affects multiple systems in mammals and is linked with greater susceptibility to bacterial infections. Chan et al. used a mouse model to show that psychological stress causes an impaired response to Staphylococcus aureus infection.

The defective response was associated with decreased dermal adipogenesis by fibroblasts and decreased production of the antimicrobial peptide cathelicidin (Camp) by these cells, thus enhancing susceptibility to S. aureus.

This brain-skin axis triggered by stress was mediated by adrenergic signaling and the production of TGFβ. These were critical for infection given that inhibiting adrenergic or TGFβ signaling restored normal host defense to S. aureus in stressed mice. ...

Abstract

Infections after psychological stress are a major health care problem.

Single-cell transcriptomics and lipidomic profiling in a mouse model of stress show that dermal fibroblasts undergoing adipogenesis have defective responses to Staphylococcus aureus skin infection.

Adrenalectomy or adrenergic inhibition restores the fibroblast adipogenic response to S. aureus and enables mice to effectively resist infection during stress. Increased susceptibility to S. aureus from stress is attributed to suppression of the antimicrobial peptide cathelicidin (Camp) because adrenaline directly inhibits Camp production by fibroblasts, and mice lacking Camp in fibroblasts do not increase infection after stress.

Transforming growth factor β (TGFβ) is induced by stress and adrenergic signaling, and inhibition of TGFβ or deletion of the TGFβ receptor on fibroblasts increases Camp expression and restores protection against infection.

Together, these data show that stress initiates a brain-skin axis mediated by TGFβ that impairs the immune defense function of dermal fibroblasts to produce the Camp antimicrobial peptide."

ScienceAdviser

Psychological stress increases skin infection through the action of TGFβ to suppress immune-acting fibroblasts (open access)

Fig. 1. Psychological stress exacerbates skin infection by SA [Staphylococcus aureus].

First testosterone patch for menopausal women boosting libido to begin clinical trials this year in the UK

Some men have too much testosterone, some women too little! Libido!

"The UK is to launch the world’s first clinical trials of a new testosterone patch aimed at boosting libido in women with symptoms of the menopause, in a move researchers believe could transform lives globally.

Testosterone is an essential hormone for women and its production drops heavily after menopause. ..."

First testosterone patch for menopausal women to begin clinical trials this year | Menopause | The Guardian UK study will look at patch’s effect on boosting libido associated with hormone level drop, which could transform lives globally

Scientists discover plant hormone that boosts growth by 30%

Amazing stuff! This could have huge implications!

"... agro-microbials—or agro-chemicals of natural origin—that can enhance the synergy between crops and microbes, and ultimately improve crop yield and productivity.

In a five-year study that began in 2018, the scientists discovered that a well-known protective hormone typically released by plants above ground during periods of stress—a volatile organic compound (VOC) known as methyl jasmonate (MeJA)—possessed a hitherto unknown function. They found that MeJa served as a shared, possibly secret, language that allows a plant to communicate with the surrounding layers of microorganisms embedded in the soil.

The research team has made three important discoveries:

1. Using a specially engineered airflow system, scientists have found, for the first time, that MeJA is released underground by the plant roots in a volatile form;
2. The presence of volatile MeJA triggers and enhances the formation of biofilms in bacteria situated at a distance from the plant roots; and
3. These bacteria in the biofilm release a different set of volatile compounds that can boost plant growth by up to 30%. ...

As the world population is projected to reach 10 billion by 2050 [I have my doubts about this projection], ensuring food security for its inhabitants has become one of the most pressing challenges of this century. Singapore, for example, has set a "30 x 30" goal—to be able to produce 30% of our nutritional needs by 2030. ..."

From the abstract:

"The rhizosphere is a niche surrounding plant roots, where soluble and volatile molecules mediate signaling between plants and the associated microbiota. The preferred lifestyle of soil microorganisms is in the form of biofilms. However, less is known about whether root volatile organic compounds (rVOCs) can influence soil biofilms beyond the 2–10 mm rhizosphere zone influenced by root exudates. We report that rVOCs shift the microbiome composition and growth dynamics of complex soil biofilms. This signaling is evolutionarily conserved from ferns to higher plants. Methyl jasmonate (MeJA) is a bioactive signal of rVOCs that rapidly triggers both biofilm and microbiome changes. In contrast to the planktonic community, the resulting biofilm community provides ecological benefits to the host from a distance via growth enhancement. Thus, a volatile host defense signal, MeJA, is co-opted for assembling host-beneficial biofilms in the soil microbiota and extending the sphere of host influence in the rhizosphere."

Scientists discover plant hormone that boosts growth by 30%

NUS-SCELSE scientists uncover plant hormone that can boost plant growth by 30% This exciting discovery holds great promise for sustainable food security across diverse soils and crops

Volatile methyl jasmonate from roots triggers host-beneficial soil microbiome biofilms

Fig. 1: Plant root VOCs promote biofilm formation in the soil microbial community.

Testosteron steigert das Wohlbefinden von Männern - viele brauchen mehr davon

Schlagzeile des Tages!

Testosteron steigert das Wohlbefinden von Männern - viele brauchen mehr davon Männer mit wenig Testosteron sind oft müde, antriebslos, niedergeschlagen und leicht reizbar. Übergewicht, Stress und Schlafmangel verursachen den Mangel in vielen Fällen.

Hormone Sobers Up Drunken Mice: Study

Good news! Let's toast to that! 😊 

"Fibroblast growth factor 21, usually abbreviated FGF21, is a hormone known to be induced by various metabolic stresses, including fasting and alcohol consumption in both humans and mice. ... Now, scientists have discovered one more property of this hormone: without it, drunk mice take longer to recover their motor skills, whereas a much larger pharmacologic dose speeds up the recovery. The effect ... is mediated by the activation of noradrenergic neurons in a region of the brainstem that regulates arousal and alertness. ..."

"A shot of a liver-produced hormone called FGF21 sobered up mice that had passed out from alcohol, allowing them to regain consciousness and coordination much faster than those that didn’t receive this treatment, ... researchers report in a new study. ..."

From the highlights and abstract:

"Highlights

• Hormone FGF21 counteracts alcohol-induced loss of consciousness and coordination

• Pharmacologic FGF21 accelerates recovery from alcohol-induced intoxication

• FGF21 exerts its sobering effect by activating the noradrenergic nervous system

Summary

Animals that consume fermenting fruit and nectar are at risk of exposure to ethanol and the detrimental effects of inebriation. In this report, we show that the hormone FGF21, which is strongly induced by ethanol in murine and human liver, stimulates arousal from intoxication without changing ethanol catabolism. Mice lacking FGF21 take longer than wild-type littermates to recover their righting reflex and balance following ethanol exposure. Conversely, pharmacologic FGF21 administration reduces the time needed for mice to recover from ethanol-induced unconsciousness and ataxia. FGF21 did not counteract sedation caused by ketamine, diazepam, or pentobarbital, indicating specificity for ethanol. FGF21 mediates its anti-intoxicant effects by directly activating noradrenergic neurons in the locus coeruleus region, which regulates arousal and alertness. These results suggest that this FGF21 liver-brain pathway evolved to protect against ethanol-induced intoxication and that it might be targeted pharmaceutically for treating acute alcohol poisoning."

 

Hormone Sobers Up Drunken Mice: Study | The Scientist Magazine® (secondary source) A hormone naturally induced by alcohol consumption accelerates the recovery of mice after binge drinking by activating neurons involved in arousal and alertness.

UT Southwestern scientists discover agent that reverses effects of intoxication (primary source) Hormone called FGF21 speeds recovery from alcohol poisoning in mice, has potential to save countless lives, researchers say

FGF21 counteracts alcohol intoxication by activating the noradrenergic nervous system (open access)

Figure 3: Pharmacologic FGF21 accelerates recovery from alcohol-induced loss of righting reflex and ataxia and is selective for ethanol

Hormone secreted when exercising halts Parkinson’s decline in mice

Good news! Exercise more! Irisin sounds like music! It was only discovered in 2012. The researchers also have show that injection of irisin may help.

"... In 2012 a team of researchers from Harvard Medical School published a landmark study reporting the discovery of a new hormone released by muscles during exercise. The researchers named the hormone irisin. ...
By 2015 the argument was ultimately settled, with new research affirming irisin is real and secreted by skeletal muscles in humans during exercise. ...
A 2019 mouse study found boosting irisin levels in Alzheimer’s animal models improved brain plasticity and memory. ..."

"Researchers from Johns Hopkins Medicine and the Dana Farber Cancer Institute in Boston have shown that a hormone secreted into the blood during endurance, or aerobic, exercise reduces levels of a protein linked to Parkinson’s disease and halts movement problems in mice. ..."

From the abstract:

"Physical activity provides clinical benefit in Parkinson’s disease (PD). Irisin is an exercise-induced polypeptide secreted by skeletal muscle that crosses the blood–brain barrier and mediates certain effects of exercise. Here, we show that irisin prevents pathologic α-synuclein (α-syn)-induced neurodegeneration in the α-syn preformed fibril (PFF) mouse model of sporadic PD. Intravenous delivery of irisin via viral vectors following the stereotaxic intrastriatal injection of α-syn PFF cause a reduction in the formation of pathologic α-syn and prevented the loss of dopamine neurons and lowering of striatal dopamine. Irisin also substantially reduced the α-syn PFF-induced motor deficits as assessed behaviorally by the pole and grip strength test. Recombinant sustained irisin treatment of primary cortical neurons attenuated α-syn PFF toxicity by reducing the formation of phosphorylated serine 129 of α-syn and neuronal cell death. Tandem mass spectrometry and biochemical analysis revealed that irisin reduced pathologic α-syn by enhancing endolysosomal degradation of pathologic α-syn. Our findings highlight the potential for therapeutic disease modification of irisin in PD."

Hormone secreted when exercising halts Parkinson’s decline in mice

Exercise Hormone Halts Parkinson’s Disease Symptoms in Mouse Study

Amelioration of pathologic α-synuclein-induced Parkinson’s disease by irisin (open access)

Testosterone — new discoveries about the male hormone

Recommendable!

Putative Exercise Hormone Irisin Boosts Mouse Brainpower

Good news! Why exercise and sweat? Can I pop a pill? (just kidding)

"The hormone irisin is necessary for the cognitive benefits of exercise in healthy mice and can rescue cognitive decline associated with Alzheimer’s disease, according to a study published August 20 in Nature Metabolism. ...
Many studies have found that exercise is good for the brain, but the molecular mechanisms responsible for the cognitive boost have remained elusive. During her postdoctoral studies, neuroscientist Christiane Wrann found that the gene that codes for irisin becomes highly expressed in the brain during exercise—one of the first studies linking irisin with the brain. ..."

From the abstract:

"Identifying secreted mediators that drive the cognitive benefits of exercise holds great promise for the treatment of cognitive decline in ageing or Alzheimer’s disease (AD). Here, we show that irisin, the cleaved and circulating form of the exercise-induced membrane protein FNDC5, is sufficient to confer the benefits of exercise on cognitive function. ...
Diminished pattern separation in F5KO mice can be rescued by delivering irisin directly into the dentate gyrus, suggesting that irisin is the active moiety. ... Importantly, elevation of circulating irisin levels by peripheral delivery of irisin via adeno-associated viral overexpression in the liver results in enrichment of central irisin and is sufficient to improve both the cognitive deficit and neuropathology in AD mouse models. Irisin is a crucial regulator of the cognitive benefits of exercise and is a potential therapeutic agent for treating cognitive disorders including AD."

Putative Exercise Hormone Irisin Boosts Mouse Brainpower | The Scientist Magazine® Mice lacking irisin didn’t exhibit the cognition improvements that typically follow exercise, and in mouse models of Alzheimer’s disease, treatment with the hormone reduced cognitive decline.

Exercise and Alzheimer’s Disease Hormone found to confer benefits of exercise on cognitive function

Exercise hormone irisin is a critical regulator of cognitive function (no public access)