A Massachusetts man became the first person to try intranasal foralumab under an expanded access program for people with moderate Alzheimer's disease, Tiziana Life Sciences said.

 With your extra risk of dementia post stroke, you doctor has a lot of work to do to prevent dementia! YOUR DOCTOR'S RESPONSIBILITY! Should you be taking this as a preventative? WHY THE FUCK WON'T YOUR DOCTOR FIND THAT OUT? Don't let your doctor weasel out of that! Your doctors have had over a decade to accomplish that! Were they competent at that or not?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018

5. Brain Bleeds Double Dementia Risk February 2025

The latest here:

A Massachusetts man became the first person to try intranasal foralumab under an expanded access program for people with moderate Alzheimer's disease, Tiziana Life Sciences said.

One paragraph from there:

Dr. Howard Weiner, Co-director of the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital, a founding member of Mass General Brigham healthcare system commented “Foralumab, administered via a novel intranasal delivery method, aims to target immune system dysregulation associated with Alzheimer’s disease, potentially slowing disease progression and improving cognitive function. The recent coverage in the News underscores the growing recognition of Foralumab’s promise in the field of neurodegenerative diseases.”

Superior cognition in individuals who are 90+ associated with resilience to neurodegenerative pathologies

 My mom who is 94, still living alone in the old house, laundry still in basement is doing pretty good yet. Still drives locally, haven't convinced her yet to get a hearing aid so repeating sentences is required.  Dad however died at 92 with Parkinson's dementia the last three years. So I'm going to live a very long time with half my life being differently abled, stroke at age 50, I'm shooting for 100+ and going to get there.

Superior cognition in individuals who are 90+ associated with resilience to neurodegenerative pathologies

A University of California, Irvine-led team of researchers have discovered that the oldest-old, those who live to be 90+ and have superior cognitive skills, have similar levels of brain pathology as Alzheimer's patients, however, they also have less brain pathology of other neurodegenerative diseases that cause memory and thinking problems.

The study, "Superior Global Cognition in Oldest-Old is Associated with Resistance to Neurodegenerative Pathologies: Results from the 90+ Study," was published in the Journal of Alzheimer's Disease.

People who are 90+ and still have good memory and thinking abilities tend to have similar levels of Alzheimer's pathology in their brains. Our findings indicate that while Alzheimer's Disease neuropathological changes and vascular changes are common in their brains, these individuals are less susceptible to other types of neurodegenerative changes such as Lewy body disease."

Roshni Biswas, post-doctoral scholar with The 90+ Study

Age is the primary risk factor for cognitive issues, such as Alzheimer's, Lewy body disease and other related dementias. Over the past 30 years, the number of people aged 90 and older in the U.S. has nearly tripled, and this number is projected to quadruple in the next four decades.

With this rise in age, many people see increased problems with memory and brain function. However, little data is available on the changes in the brains of 90+ people who maintain superior cognitive abilities, despite their age.

The objective of the study was to examine the brain features of people without cognitive impairment and their relation to superior cognitive skills and reasoning in those that are 90+.

"There are some individuals who can maintain high levels of cognitive function well into advanced ages," said María M. Corrada, ScD, co-principal investigator of the study and professor in the Department of Neurology at UCI School of Medicine. "Further research into the factors that enable these individuals to maintain their cognitive function could provide insights into how to preserve cognitive health despite advanced age."

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The study results were derived by analyzing autopsy data from 102 cognitively normal individuals who died at a mean age of 97.6 years. They also used cognitive test scores from people taken between two to twelve months before death. The average age of study participants at the time of their last visit was 97.1 years of age.

"In our future research, we will examine how lifestyle habits and health conditions are associated with superior cognition in individuals who are 90+ and the factors that contribute to maintaining stable cognitive function over time," said Biswas.

The 90+ Study is a longitudinal study on aging and dementia that was initiated in 2003 to study the oldest-old population, which is the fastest growing age group in the United States.

With more than 2000 participants enrolled, it is now one of the largest studies of its kind in the world. The project has produced several significant findings regarding cognitive function, health and lifestyle habits in the oldest-old population information obtained during life.

This work was supported by the National Institutes of Health.

Source:

University of California - Irvine

Journal reference:

Biswas, R., et al. (2023) Superior Global Cognition in Oldest-Old is Associated with Resistance to Neurodegenerative Pathologies: Results from the 90+ Study. Journal of Alzheimer s Disease. doi.org/10.3233/JAD-221062.

Long COVID may progress into neurodegenerative disease

So get vaccinated.

 Long COVID may progress into neurodegenerative disease

Edible mushrooms: the role of antioxidant compounds as potential candidates for neurodegenerative disease prevention and treatment

Hell, hasn't your doctor years ago had the dietician create a diet protocol on mushrooms? NO? Then you don't have a functioning stroke doctor.

• magic mushrooms (23 posts to October 2014)

• mushrooms (14 posts to October 2014)

Edible mushrooms: the role of antioxidant compounds as potential candidates for neurodegenerative disease prevention and treatment

• Download PDF Copy

By Pooja Toshniwal PahariaApr 18 2023Reviewed by Lily Ramsey, LLM

In a recent review published in the Nutrients Journal, researchers reviewed existing data on edible mushrooms as dietary sources of antioxidants for preventing neurodegenerative diseases (NDs) associated with aging.

Study: Antioxidant Compounds from Edible Mushrooms as Potential Candidates for Treating Age-Related Neurodegenerative Diseases. Image Credit: FotoHelin/Shutterstock.com

Background

Edible mushrooms reportedly produce different antioxidant compounds such as polysaccharides, flavonoids, phenolics, ergothioneine, carotenoids, and vitamins.

Therefore, mushrooms may be used as dietary supplements to improve antioxidant defenses and prevent age-associated NDs, characterized by increased oxidative stress, especially among older adults.

About the study

In the present study, researchers presented the role of oxidative stress in age-associated NDs and the potential of edible mushrooms to preserve healthy aging.

Role of oxidative stress in health, aging, and neurodegenerative diseases

In healthy conditions, reactive oxygen species (ROS)/RNS are balanced by efficient defense mechanisms. However, the oxidant levels increase during aging, while the antioxidant defenses become less efficient, generating an imbalance that leads to oxidative stress.

The condition results in oxidative damage to the main biomolecules, leading to the development of age-related neurodegenerative conditions such as Alzheimer’s and Parkinson’s diseases.

The hallmarks of aging include cellular senescence, telomere shortening, genomic instability, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, stem cell exhaustion, and altered intracellular communication.

An increase in oxidative stress with advancing age could result in mitochondrial dysfunction, lipid peroxidation, lipid membrane alterations, protein oxidation, deoxyribonucleic acid (DNA) and messenger ribonucleic acid (mRNA) damage, chronic inflammation, and cell death.

As a consequence, NDs may develop, with increased Aβ and α-synuclein protein deposition, neuroinflammation, and neuronal dysfunction.

Antioxidant mycochemicals of edible and medicinal mushrooms

Antioxidants obtained from edible mushrooms include flavonoids, phenolics, vitamins (α, β, γ, δ-tocopherol and tocoretinol, and ascorbic acid), carotenoids (α- and β-carotene, and β-cryptoxanthin), polysaccharides (pleuran, lentinan, and β-glucan), and ergothioneine. Which prevent damage by free radicals, including peroxynitrite (ONOO-), O2-, nitric oxide (NO), and hydroxyl (OH).

Forensics And Toxicology eBook Compilation of the top interviews, articles, and news in the last year. Download the latest edition

Mushrooms also provide minerals such as potassium (K), phosphorus (P), magnesium (Mg), sodium (Na), calcium (Ca), zinc (Zn), manganese (Mn), iron (Fe), copper (Cu), cobalt (Co), nickel (Ni), selenium (Se), and glutathione (GSH).

The antioxidants increase longevity, improve overall health, and reduce cell death and inflammation to prevent the development of age-associated NDs. Agaricus bisporus fungi contain acid-retrievable polysaccharides (AcAPS) that have prevented hydroxyl- and diphenyl-1-picrylhydrazyl (DPPH)-induced damage in vitro and conferred nephric and hepatic protection by enhancing serological enzymatic activity in aged mice, in vivo.

Endo-polysaccharides (EnPS) and exopolysaccharides (ExPS) have been obtained from Agaricus brasiliensis, with similar properties in vitro, in addition to an improvement in total antioxidant capacity (TAC) with lowered malondialdehyde (MDA) content.

Agrocybe aegerita contains alkalic-retrievable and acid-retrievable mycelia polysaccharides (Al-MPS and Ac-MPS) that can scavenge DPPH and hydroxyl activities, increase superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and TAC, decrease MDA content, and reduce lipid peroxidation.

Agrocybe aegerita intake has reduced serological triglyceride and cholesterol levels in aged mice. Agrocybe cylindracea, comprising the SL-02 selenium polysaccharide and exopolysaccharides (EPS), has demonstrated similar properties.

Sulfated polysaccharides (SFPS) in Flammulina velutipes can scavenge DPPH, hydroxyl, and superoxide radicals, chelate iron, lower lipid peroxidation, and improve anti-inflammatory responses.

Ganoderma lucidum comprises polysaccharides that lower amyloid toxicity, neurotoxicity, MDA content, microglial activation, interleukin-1 beta (IL-1β), and tumor necrosis factor-alpha (TNF-α) levels.

In addition, the antioxidants increase GSH and GPx activity to prevent dopaminergic neuronal inflammation. Grifola frondose comprises polysaccharides (GFP), including intracellular-type Zn polysaccharides (IZPS). Hericium erinaceus comprises sulfated residue polysaccharide (SHRP) compounds that scavenge free radicals and lower MDA content.

The antioxidants in Lentinula edodes (MPS with and without zinc), Lepista sordida (CLSP polysaccharides), and Pholiota nameko (Zn-rich MZPS polysaccharides) have demonstrated similar properties.

Pleurotus eryngii comprises polysaccharides (PEP) and enzymatic residue polysaccharides (PERP) that have shown neuroprotective activity, preventing β-amyloid-inflicted neurotoxicity among rats, improving the functioning of the liver, skin, and brain, in vivo.

Similarly, consuming Pleurotus ostreatus, comprising polysaccharides (POP), and Pleurotus sajor-caju, comprising the PSP2-1 polysaccharide, improved cognition in rats with Alzheimer’s disease, reducing MDA and acetylcholinesterase (AchE) activity.

Polysaccharide TFPS, in Tremella fuciformis, improves hydrogen peroxide-caused oxidative-type stress and inhibits apoptosis among human cutaneous fibroblasts through sirtuin 1 (SIRT1) upregulation.

Increased CAT and SOD activity has been observed in aged murine animals that consumed Tricholoma lobayense, comprising TLH-3 polysaccharide.

Conclusions

Based on the review findings, edible and medicinal mushrooms are safe and non-toxic foods that comprise various antioxidants that can prevent neurodegeneration among aged individuals, particularly ergothioneine and polysaccharides. Vitamins and phenolics may act synergistically to counteract oxidative damage and preserve brain health.

Additionally, most human studies used whole mushrooms, powders, or extracts and did not assess the health-promoting effects of isolated compounds.

However, studies involving humans to evaluate the neuroprotective effects of mushrooms are limited, warranting further research to assess mushroom-induced neuroprotection, elucidate the underlying molecular neuroprotective mechanisms, and define optimal intake levels.

Journal reference:

• Liuzzi, G. et al. (2023) "Antioxidant Compounds from Edible Mushrooms as Potential Candidates for Treating Age-Related Neurodegenerative Diseases", Nutrients, 15(8), p. 1913. doi: 10.3390/nu15081913. https://www.mdpi.com/2072-6643/15/8/1913

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Tags: Aging, Anti-Inflammatory, Antioxidant, Apoptosis, Ascorbic Acid, Brain, Calcium, Cell, Cell Death, Cholesterol, Chronic, Copper, DNA, Dopaminergic, Exhaustion, Free Radicals, fungi, Genomic, Hydrogen Peroxide, in vitro, in vivo, Inflammation, Interleukin, Intracellular, Liver, Magnesium, Manganese, Membrane, Minerals, Mushroom, Necrosis, Neurodegeneration, Neurodegenerative Disease, Neurodegenerative Diseases, Nitric Oxide, Nutrients, Oxidative Stress, Oxygen, Potassium, Protein, Proteostasis, Research, Ribonucleic Acid, Selenium, Skin, Stress, Supplements, Telomere, Triglyceride, Tumor, Tumor Necrosis Factor, Vitamins, Zinc

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Pooja Toshniwal Paharia

Dr. based clinical-radiological diagnosis and management of oral lesions and conditions and associated maxillofacial disorders.

FDA releases 5-year action plan to combat neurodegenerative diseases

Because we have fucking failures of stroke associations  we are getting nothing to help the hundreds of thousands of yearly stroke survivors in the US.

FDA releases 5-year action plan to combat neurodegenerative diseases

By Ken Downey Jr.

Source/Disclosures

ADD TOPIC TO EMAIL ALERTS

The FDA on June 23 announced a 5-year strategy for improving and extending the lives of people with rare neurodegenerative diseases by advancing development of safe and effective medical products and facilitating access to novel treatments.

The plan, which will serve as a blueprint for how the agency will move forward in tackling challenges in drug development, was developed in accordance with the Accelerating Access to Critical Therapies for ALS Act that President Joe Biden signed into law in December 2021, the FDA said in a press release.

Source: Adobe Stock.

“The effects of rare neurodegenerative diseases are devastating, with very few effective therapeutic options available to patients,” FDA Commissioner Robert M. Califf, MD, said in the release. “We recognize the urgent need for new treatments that can both improve and extend the lives of people diagnosed with these diseases.”

According to the release, during the 5-year span, the plan will focus on bolstering scientific advancement and promoting innovation by:

• establishing the FDA Rare Neurogenerative Disease Task Force;
• establishing the public-private partnership for rare neurodegenerative diseases;
• developing disease-specific science strategies; and
• leveraging ongoing FDA regulatory science efforts.

A key focus of the plan is the ALS Science Strategy, which provides a forward-learning framework for FDA activities to assess key regulatory science priorities. Highlights of the strategy include:

• improving characterization of disease pathogenesis and natural history;
• facilitating patient access to new drugs whenever possible and promoting greater participation in clinical trials by reducing barriers and burdens faced by minority populations; and
• enhancing clinical trial infrastructure and agility to enable early selection of promising therapeutic candidates for further development, optimizing clinical trial design, improving access to the trials, streamlining trail operations and reducing the time and cost of drug development.

Per the release, success of the FDA’s implementation of the ALS Science Strategy will rely on patient engagement, public workshop, research projects and collaboration with the NIH.

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“To face that challenge and to accelerate drug development, we need innovative approaches to better understand these diseases while also building on current scientific and research capabilities,” Califf said. “This action plan, especially including the use of public-private partnerships and direct involvement of patients, will ensure the FDA is working toward meeting the task set forth by Congress to enhance the quality of life for those suffering by facilitating access to new therapies.”

 

Sorting protein in neurons defends against neurodegenerative disease

You will need this. SO DEMAND TO KNOW FROM YOUR DOCTOR AND STROKE HOSPITAL WHAT THEY ARE DOING TO ENSURE THIS CREATES A PREVENTION PROTOCOL FOR YOUR USE.  

Tauopathy has been out there since July 2012. How fucking long will you allow your doctor and stroke hospital to continue this incompetence? After your children and grandchildren have strokes? 

• tauopathy (2 posts back to July 2012)

 

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018

The latest here.

Sorting protein in neurons defends against neurodegenerative disease

by Temple University

Domenico Praticò, MD, Scott Richards North Star Foundation Chair for Alzheimer's Research, Professor in the Departments of Pharmacology and Microbiology, and Director of the Alzheimer's Center at Temple at the Lewis Katz School of Medicine at Temple University Credit: Lewis Katz School of Medicine at Temple University

Like a sorting machine in an assembly line, a molecule known as VPS35 detects and removes defective proteins from neurons. And similar to other quality control processes, the VPS35 system goes a long way toward protecting health, according to new work by researchers at the Lewis Katz School of Medicine at Temple University. They show for the first time that VPS35 clears the brain of a potentially harmful protein called tau, which otherwise accumulates and contributes to neurodegenerative disorders, including Alzheimer's disease.

The new findings were published online July 9 in the journal Molecular Psychiatry.
"A major part of what VPS35 does is to sort out and transport dysfunctional proteins to degradation sites," explained senior investigator Domenico Praticò, MD, Scott Richards North Star Foundation Chair for Alzheimer's Research, Professor in the Departments of Pharmacology and Microbiology, and Director of the Alzheimer's Center at Temple at the Lewis Katz School of Medicine (LKSOM).
The buildup of defective proteins in neurons is a feature shared by Alzheimer's disease, Parkinson's disease, and several other neurodegenerative conditions. Tau is one of the major proteins to amass in the brain and cause damage in these diseases, creating a condition described as tauopathy.
Previous work by other researchers had shown that the function of VPS35 is altered in Alzheimer's disease and that VPS35 activity is reduced in the brains of Alzheimer's patients. The relationship between VPS35 activity and tau accumulation was largely unexplored.
"We asked specifically whether the VPS35 system is important for clearing defective tau proteins," Dr. Praticò said. To answer this question, his team of researchers examined brain tissue from patients with either progressive supra-nuclear palsy (PSP) or Picks' disease. Unlike Alzheimer's disease, in which tau accumulation is secondary to that of beta-amyloid, in PSP and Picks' disease tau is the only protein to form deposits in the brain.
Analyses revealed that the brains of PSP and Pick's disease patients had VPS35 levels that were 50 percent lower than those of control subjects. When the researchers deliberately altered VPS35 levels in individual tauopathy-affected neurons in vitro, they discovered that they could directly control tau accumulation, for the first time implicating VPS35 in tauopathy. The VPS35-dependent effect on tau was mediated by the activity of cathepsin D, an enzyme that specializes in protein degradation.
Dr. Praticò's team also carried out experiments in mice with tau accumulation. VPS35 downregulation in these animals exacerbated memory and learning impairment and was associated with worsened motor function. Moreover, VPS35 reduction resulted in a loss of synaptic integrity between neurons in the animals' brains, significantly damaging neural communication.
"When tau lingers in cells, it is very bad for synapses, the places where neurons meet and exchange signals," explained Dr. Praticò. "In the animals we studied, there was a 40 to 50 percent loss in synaptic connectivity when VPS35 activity was reduced, which led to the types of cognitive and motor deterioration, including losses in memory and learning ability, seen in human tauopathy patients."
The discovery of the involvement of cathepsin D shed additional light on the relationship between VPS35 and tau. "Without VPS35, cathepsin D does not degrade tau, leaving tau to build up in the brain," Dr. Praticò said.
Dr. Praticò's team plans next to investigate the possibility of using a drug to put VPS35 back to work in the context of neurodegenerative disease. "The approach would be unique. Instead of targeting an enzyme, as other small molecules have been developed to do, we would be targeting an actual mechanism, which should be more viable," he said.

Felodipine, FDA-Approved for Blood Pressure, Shows Promise in Dementia

It is YOUR RESPONSIBILITY to get your doctor and stroke hospital involved with initiating research into human subjects on this. Your stroke hospital will do nothing if you don't speak up. Because your stroke hospital has done no followup for decades is the reason nothing is ever solved in stroke.  Does your stroke hospital even know that stroke survivors need this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018

 

Felodipine, FDA-Approved for Blood Pressure, Shows Promise in Dementia

At the University of Cambridge, a prescribed drug to treat high blood pressure has shown promise against conditions such as Parkinson's, Huntington's and forms of dementia in studies carried out in mice and zebrafish.

A common feature of these diseases -- collectively known as neurodegenerative diseases -- is the build-up of misfolded proteins. These proteins, such as huntingtin in Huntington's disease and tau in some dementias, form 'aggregates' that can cause irreversible damage to nerve cells in the brain.

Autophagy Protects Brain Cells

In healthy individuals, the body uses a mechanism to prevent the build-up of such toxic materials. This mechanism is known as autophagy, or 'self-eating', and involves 'Pac-Man'-like cells eating and breaking down the materials. However, in neurodegenerative diseases this mechanism is impaired and unable to clear the proteins building up in the brain.

As the global population ages, an increasing number of people are being diagnosed with neurodegenerative diseases, making the search for effective drugs ever more urgent. However, there are currently no drugs that can induce autophagy effectively in patients.

Re-purpose Existing Drugs

In addition to searching for new drugs, scientists often look to re-purpose existing drugs. These have the advantage that they have already been shown to be safe for use in humans. If they can be shown to be effective against the target diseases, then the journey to clinical use is much faster.

In a study published today in the journal Nature Communications, scientists at the UK Dementia Research Institute and the Cambridge Institute for Medical Research at the University of Cambridge have shown in mice that felodipine, a hypertension drug, may be a candidate for re-purposing.

Felodipine Seems to Induce Autophagy

Epidemiological studies have already hinted at a possible link between the drug and reduced risk of Parkinson's disease, but now the researchers have shown that it may be able to induce autophagy in several neurodegenerative conditions.

A team led by Professor David Rubinsztein used mice that had been genetically modified to express mutations that cause Huntington's disease or a form of Parkinson's disease, and zebrafish that model a form of dementia.

Mice are a useful model for studying human disease as their short life span and fast reproductive rate make it possible to investigate biological processes in many areas. Their biology and physiology have a number of important characteristics in common with those of humans, including similar nervous systems.

Felodipine Reduces Sign of Dementia

Felodipine was effective at reducing the build-up of aggregates in the mice with the Huntington's and Parkinson's disease mutations and in the zebrafish dementia model. The treated animals also showed fewer signs of the diseases.

Studies in mice often use doses that are much higher than those known to be safe to use in humans. Professor Rubinsztein and colleagues showed in the Parkinson's mice that it is possible to show beneficial effects even at concentrations similar to those tolerated by humans. They did so by controlling the concentrations using a small pump under the mouse's skin.

First Time Approved Drug Slows Buildup

"This is the first time that we're aware of that a study has shown that an approved drug can slow the build-up of harmful proteins in the brains of mice using doses aiming to mimic the concentrations of the drug seen in humans," says Professor Rubinsztein. "As a result, the drug was able to slow down progression of these potentially devastating conditions and so we believe it should be trialed in patients."

"This is only the first stage, though. The drug will need to be tested in patients to see if it has the same effects in humans as it does in mice. We need to be cautious, but I would like to say we can be cautiously optimistic."

REFERENCE:

• Siddiqi, FH et al. Felodipine induces autophagy in mouse brains with pharmacokinetics amenable to repurposing. Nature Communications; 18 April 2019; DOI: 10.1038/s41467-019-09494-2

SUPPORT:

• The study was funded by Wellcome, the Medical Research Council, Alzheimer’s Research UK, the Alzheimer’s Society, Rosetrees Trust, The Tau Consortium, an anonymous donation to the Cambridge Centre for Parkinson-Plus, Open Targets, the Guangdong Province Science and Technology Program, with additional support from the National Institute for Health Research Cambridge Biomedical Research Centre.

SOURCE:

• University of Cambridge

New robotic system can diagnose neurodegenerative diseases through eye movements

And after it is diagnosed you can use this:  

Scientists hope they have found a drug to stop all neurodegenerative brain diseases, including dementia April, 2017 

 

Assuming your doctor didn't drop the ball and did nothing to get it tested in humans.

 

New robotic system can diagnose neurodegenerative diseases through eye movements

• Download PDF Copy

June 13, 2018

A new robotic system developed by UPM researchers and AURA Innovative Robotics Company can help diagnose neurodegenerative diseases, such as dementia and Parkinson, through the analysis of eye movements.
OSCANN Desk is a non-invasive technology developed by researchers from Universidad Politécnica de Madrid (UPM) and the company AURA Innotive Robotics, led by Cecilia García Cena that with a simple and fast test can provide data about brain functioning through the measurement of eye movements.
This new system is in the phase of clinical trial authorized by the Spanish Agency of Medicines and Medical Devices in six Spanish hospitals and, thanks to techniques of imaging processing and machine learning, its results will allow doctors to early diagnose neurodegenerative diseases and carry out customized treatments.
The diagnosis process of a neurodegenerative disease takes time since symptoms are complex to assess in the early stages of the disease. Besides, there are symptoms that are common to other neurodegenerative diseases such as tremors. High rates of diagnostic uncertainty make objective tests necessary to achieve an accurate medicine in which each patient receives information, prognosis and appropriate treatment.
The physiological process in medicine explains the eye movements. To accurately measure these movements would provide real-time information about how the brain is working at that moment. From this premise and in order to achieve an early diagnosis of neurodegenerative diseases, researchers from Centre for Automation and Robotics (CAR) CSIC-UPM and AURA Innovative Robotics Startup Company have developed OSCANN desk, an assistant medical device that through techniques of image processing and machine learning is able to accurately assess the eye movements.
Thanks to this new tool, doctors will have objective data of the brain functioning that, along with other clinical data, will use to carry out an accurate early diagnosis of the disease.
The test is conducted in a health care center with no need for a second doctor's appointment. The personnel select a set of calibration and tests of each patient. The patient sits comfortably in a chair and the device is adapted to his anatomy to precisely measure the eye movement. The patient has to look at the stimulus that appears on a monitor, each test lasts about a minute.

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The clinical tests allowed researchers to develop models of pathologies and, by applying machine learning techniques, similarities and differences are searched among over 500 variables of eye movement. Likewise, the progress of certain symptoms can be objectively measured. This will help doctors to make a diagnosis and customize the treatment.
Today, the tests are applied to Alzheimer's, Parkinson's, mild cognitive impairment, diverse dementias, multiple sclerosis, etc. Besides, researchers are collaborating in other clinical research such as autistic spectrum disorders, epilepsy, diabetes, alcoholism, migraines, depression and bipolar disorder. This tool is being used in six hospitals that are national reference centers in pathologies: Hospital Universitario 12 de Octubre, Hospital Sant Pau, Hospital Clinic de Valencia, Hospital Clinic de Barcelona, Hospital Marqués de Valdecilla and Hospital Valle de Hebrón. Besides, the Centro de Investigaciones Príncipe Felipe is collaborating in the project.
In a near future, OSCANN Desk will be working in HM Hospitals, specifically in the Memory Disorders Unit of HM CINAC located at the Hospital Universitario HM Madrid.

Source:

http://www.upm.es/internacional/UPM/UPM_Channel/Research_News?id=a1f94820678f3610VgnVCM10000009c7648a____&fmt=detail&prefmt=articulo

Study Shows Air Pollution Makes Genetic Changes in the Brain

So for your recovery from stroke your doctor should be prescribing clean air along with forest bathing and visiting the beach. Does your doctor prescribe anything for your recovery except for E.T.(Evaluate and Treat) to your PT, OT and ST?  That prescription means your doctor knows nothing about stroke recovery.
https://www.sierraclub.org/sierra/study-shows-air-pollution-makes-genetic-changes-brain?

By Jason Daley | Jun 6 2018

There’s little question that air pollution is toxic for the human body. Studies have shown that particulate matter in the air can lead to lung disease, heart disease, strokes, and lung cancer. But researchers thought the brain might be protected due to the blood brain barrier—a natural system that filters out foreign substances and certain neurotransmitters before they circulate in the brain. A new study from researchers at Cedars-Sinai Medical Center in Los Angeles shows that many heavy metals found in the air may make it into brain tissue, and those pollutants are activating genes that may lead to cancers or neurodegenerative disorders. 

To understand how air pollution impacts the brain, doctor Julia Ljubimova, director of the Nanomedicine Research Center at Cedars-Sinai, produced air with the same chemical makeup as that found in Riverside, California, in the Los Angeles Basin. She and her team then subjected rats to the air, with different groups of rats breathing the polluted air for two weeks, one to three months, and 12 months. After examining the rodent brains, the researchers found higher than normal concentrations of heavy metals including cadmium, cobalt, lead, nickel, vanadium, and zinc accumulated in the rats exposed to the pollution for a month or more. Even more disturbing, coarse particles of the pollutants had switched on certain genes. The research appears in the journal Scientific Reports. 

“Initially I was even skeptical we could find anything. For example, a smoker has to smoke 20 years to develop lung cancer,” Ljubimova says, “so I was not sure that in three, six, or 12 months of exposure we would detect changes in these animals’ brains at the genomic level. I was very, very surprised when we found so many changes.”

So how are these heavy metals making it into the brain despite the blood brain barrier? The coarse particulate material gets in through the lungs, which absorb the pollution particles into the bloodstream and may somehow beat the blood brain barrier, which can weaken due to high blood pressure, inflammation, and other stresses. Particulates inhaled through the nose have a more direct route into the brain through the olfactory system and may accumulate through that pathway. Once in the brain, the metals cause inflammation, switching on certain genes including those that cause both benign and malignant tumors, and others that are suspected of causing neurodegenerative disorders like Parkinson’s, ALS, Alzheimer’s, and other types of dementia—something that other recent studies have also found.

There are still many questions the study can’t answer. For instance, do these heavy metals accumulate throughout a lifetime, or can the body flush them out? And most importantly, can a study on rats translate to humans? While Ljubimova says it’s likely that the same systems are at work in humans and rodents, her team is also studying Cedars-Sinai’s archive of human brain tissue to see if there’s evidence of these coarse particles accumulating in the brains of people who lived in areas with air pollution.

Ljubimova says that while the pollutants in her study were based on Los Angeles, she guesses many of the same effects are happening in cities across the world with similar loads of coarse pollutants. The hope, she says, is that the study and future follow-ups will galvanize policymakers to take a closer look at the health impacts of industry, auto emissions, agriculture, and military activities in L.A. and other areas with pollution problems. She points out that more and more people are being exposed to questionable air as urbanization expands, and scientists don’t know all the possible organs and ill effects exposure can cause. 

“We thought that nature protected the brain through the blood brain barrier,” she says. “But now we see that no, air pollution affects even isolated and protected organs such as the brain. This is important information for thinking about new developments and ways to protect the public.”

Scientists hope they have found a drug to stop all neurodegenerative brain diseases, including dementia

With a great stroke association we could join these researchers in finding a feasible solution. But that will never occur until we destroy the existing fucking failures of stroke associations. NO LEADERSHIP AND NO STRATEGY from them.
You need this solution and soon.
1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.

Scientists hope they have found a drug to stop all neurodegenerative brain diseases, including dementia

In 2013, a UK Medical Research Council team stopped brain cells dying in an animal for the first time, creating headline news around the world.
But the compound used was unsuitable for people, as it caused organ damage.
Now two drugs have been found that should have the same protective effect on the brain and are already safely used in people.
"It's really exciting," said Prof Giovanna Mallucci, from the MRC Toxicology Unit in Leicester.
She wants to start human clinical trials on dementia patients soon and expects to know whether the drugs work within two to three years.

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Why might they work?

The novel approach is focused on the natural defence mechanisms built into brain cells.
When a virus hijacks a brain cell it leads to a build-up of viral proteins.
Cells respond by shutting down nearly all protein production in order to halt the virus's spread.
Many neurodegenerative diseases involve the production of faulty proteins that activate the same defences, but with more severe consequences.
The brain cells shut down production for so long that they eventually starve themselves to death.
This process, repeated in neurons throughout the brain, can destroy movement, memory or even kill, depending on the disease.
It is thought to take place in many forms of neurodegeneration, so safely disrupting it could treat a wide range of diseases.
In the initial study, the researchers used a compound that prevented the defence mechanism kicking in.
It halted the progress of prion disease in mice - the first time any neurodegenerative disease had been halted in any animal.
Further studies showed the approach could halt a range of degenerative diseases.
The findings were described as a "turning point" for the field even though the compound was toxic to the pancreas.

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Neurodegeneration

• A neurodegenerative disease is one in which the cells of the brain and spinal cord are lost
• The functions of these cells include decision making and control of movements
• These cells are not easily regenerated, so the effects of diseases can be devastating
• Neurodegenerative diseases include Alzheimer's, Parkinson's, multiple sclerosis and Huntington's

Source: London Brain Centre

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Safe drugs?

Since 2013, the research group has tested more than 1,000 ready-made drugs on nematode worms, human cells in a dish and mice.
Two were shown to prevent both a form of dementia and prion disease by stopping brain cells dying.
Prof Mallucci told the BBC News website: "Both were very highly protective and prevented memory deficits, paralysis and dysfunction of brain cells."
The best known drug of the pair is trazodone, which is already taken by patients with depression.
The other, DBM, is being tested in cancer patients.
Prof Mallucci said: "It's time for clinical trials to see if there's similar effects in people and put our money where our mouth is.
"We're very unlikely to cure them completely, but if you arrest the progression you change Alzheimer's disease into something completely different so it becomes liveable with."
But, although trazodone is a current medication, she added: "As a professional, a doctor and a scientists, I must advise people to wait for the results."

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What do the experts think?

Dr Doug Brown, from the Alzheimer's Society, said: "We're excited by the potential of these findings, from this well conducted and robust study.
"As one of the drugs is already available as a treatment for depression, the time taken to get from the lab to the pharmacy could be dramatically reduced."
Dr David Dexter, from Parkinson's UK, said: "This is a very robust and important study.
"If these studies were replicated in human clinical trials, both trazodone and DBM could represent a major step forward."

New review examines potential of antioxidant therapies to combat neurodegenerative disorders

Would anything here help stroke recovery? 

New review examines potential of antioxidant therapies to combat neurodegenerative disorders

A new review examines the potential of antioxidant approaches for the treatment of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis.
Certain compounds that are involved in oxidative stress look like promising therapeutic targets. For example, researchers are investigating the potential of increasing antioxidant capacity by targeting what's known as the Nrf2 pathway, as well as developing inhibitors of NADPH oxidases, which are key sources of reactive oxygen species. Other potential strategies for limiting oxidative stress in neurodegenerative diseases include reducing the production of nitric oxide, or preventing mitochondrial dysfunction.
"There are still several gaps in our understanding of the basis of oxidative damage in neurodegenerative disorders; however, it is increasingly accepted that many diseases share common pathways of oxidative stress-related damage, and it's likely that significant progress will be made in the design and implementation of effective therapeutic strategies in the next few years," said Dr. Gethin McBean, lead author of the British Journal of Pharmacology review.

Source:

Wiley

Neuroprotective effects of the catalytic subunit of telomerase: A potential therapeutic target in the central nervous system

No clue. You could ask our fucking failures of stroke associations but they won't even know about it much less do any followup research. In case you haven't figured it out yet, you're screwed, your children and grandchildren are screwed unless we destroy the existing stroke organizations and replace them with survivor focused ones.
http://www.ncbi.nlm.nih.gov/pubmed/27095058

González-Giraldo Y¹, Forero DA², Echeverria V³, Gonzalez J¹, Ávila-Rodriguez M⁴, Garcia-Segura LM⁵, Barreto GE⁶.

Author information

Abstract

Senescence plays an important role in neurodegenerative diseases and involves key molecular changes induced by several mechanisms such as oxidative stress, telomere shortening and DNA damage. Potential therapeutic strategies directed to counteract these molecular changes are of great interest for the prevention of the neurodegenerative process. Telomerase is a ribonucleoprotein composed of a catalytic subunit (TERT) and a RNA subunit (TERC). It is known that the telomerase is involved in the maintenance of telomere length and is a highly expressed protein in embryonic stages and decreases in adult cells. In the last decade, a growing number of studies have shown that TERT has neuroprotective effects in cellular and animal models after a brain injury. Significantly, differences in TERT expression between controls and patients with major depressive disorder have been observed. More recently, TERT has been associated with the decrease in reactive oxygen species and DNA protection in mitochondria of neurons. In this review, we highlight the role of TERT in some neurodegenerative disorders and discuss some studies focusing on this protein as a potential target for neuroprotective therapies. (We don't need discussion, we need followup research and if we had a strategy we could get somewhere by following a strategy.)

Cerium oxide nanoparticles promote neurogenesis and abrogate hypoxia-induced memory impairment through AMPK–PKC–CBP signaling cascade

Sounds extremely useful in stroke. Whom is going to follow this up in humans?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4818056/

Aditya Arya,¹ Anamika Gangwar,¹ Sushil Kumar Singh,² Manas Roy,^3,4 Mainak Das,³ Niroj Kumar Sethy,¹ and Kalpana Bhargava¹

Author information ► Copyright and License information ►

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Abstract

Structural and functional integrity of the brain is adversely affected by reduced oxygen saturation, especially during chronic hypoxia exposure and often encountered by altitude travelers or dwellers. Hypoxia-induced generation of reactive nitrogen and oxygen species reportedly affects the cortex and hippocampus regions of the brain, promoting memory impairment and cognitive dysfunction. Cerium oxide nanoparticles (CNPs), also known as nanoceria, switch between +3 and +4 oxidation states and reportedly scavenge superoxide anions, hydrogen peroxide, and peroxynitrite in vivo. In the present study, we evaluated the neuroprotective as well as the cognition-enhancing activities of nanoceria during hypobaric hypoxia. Using polyethylene glycol-coated 3 nm nanoceria (PEG-CNPs), we have demonstrated efficient localization of PEG-CNPs in rodent brain. This resulted in significant reduction of oxidative stress and associated damage during hypoxia exposure. Morris water maze-based memory function tests revealed that PEG-CNPs ameliorated hypoxia-induced memory impairment. Using microscopic, flow cytometric, and histological studies, we also provide evidences that PEG-CNPs augmented hippocampus neuronal survival and promoted neurogenesis. Molecular studies revealed that PEG-CNPs promoted neurogenesis through the 5′-adenine monophosphate-activated protein kinase–protein kinase C–cyclic adenosine monophosphate response element-binding protein binding (AMPK-PKC-CBP) protein pathway. Our present study results suggest that nanoceria can be translated as promising therapeutic molecules for neurodegenerative diseases.

Real maple syrup shows promise in protecting brain health

Look at the source of the data.
http://www.news-medical.net/news/20160314/Real-maple-syrup-shows-promise-in-protecting-brain-health.aspx

As part of a two-day symposium at the annual meeting of the American Chemical Society, a group of international scientists shared promising results of 24 studies exploring the beneficial effects of natural products on the prevention of neurodegenerative diseases, particularly Alzheimer's disease. For the first time at this symposium, real maple syrup was included among the healthful, functional foods that show promise in protecting brain cells against the kind of damage found in Alzheimer's disease.
One study presented by Dr. Donald Weaver, from the Krembil Research Institute of the University of Toronto, found that an extract of maple syrup may help prevent the misfolding and clumping of two types of proteins found in brain cells - beta amyloid and tau peptide. When cellular proteins fold improperly and clump together, they accumulate and form the plaque that is involved in the pathogenesis of Alzheimer's and other brain diseases.
The other research presented at the symposium showed that a pure maple syrup extract prevented the fibrillation (tangling) of beta amyloid proteins and exerted neuroprotective effects in rodent's microglial brain cells. Scientists have found that a decrease in microglial brain cell function is associated with Alzheimer's disease and other neurological problems. The maple syrup extract also prolonged the lifespan of an Alzheimer's roundworm model in vivo. The study was conducted out of the University of Rhode Island, in collaboration with researchers at Texas State University, and was led by Dr. Navindra P. Seeram, the symposium's organizer.
"Natural food products such as green tea, red wine, berries, curcumin and pomegranates continue to be studied for their potential benefits in combatting Alzheimer's disease. And now, in preliminary laboratory-based Alzheimer's disease studies, phenolic-enriched extracts of maple syrup from Canada showed neuroprotective effects, similar to resveratrol, a compound found in red wine," said Dr. Seeram. "However, further animal and eventually human studies would be required to confirm these initial findings."

These preliminary findings help support discoveries made over the past few years on the inherent properties of pure maple syrup that comes directly from the sap of the maple tree, making it an all-natural product with unique health benefits.
Serge Beaulieu, President of the Federation of Quebec Maple Syrup Producers, is excited by the findings of the independent scientific studies and enthusiastic about the potential pure maple syrup may have on neurological health. "The Federation and the 7300 Quebec maple enterprisers are committed to investing in scientific research to help better understand the link between food and health. This has been demonstrated by a robust and carefully guided research program that started in 2005 to explore the potential health benefits of pure maple syrup," said Beaulieu. "We already know that maple has more than 100 bioactive compounds, some of which have anti-inflammatory properties. Brain health is the latest topic of exploration and we look forward to learning more about the potential benefits that maple syrup might have in this area."
Alzheimer's disease is a progressive, neurodegenerative disease that impairs daily functioning through gradual loss of memory. Alzheimer's has no current cure, but treatments for symptoms are available and research continues. According to the Alzheimer's Association, every 67 seconds, someone in the U.S. develops Alzheimer's disease, a condition that currently cannot be cured, prevented or even slowed. It is the sixth leading cause of death in the U.S., afflicts 11 percent of the U.S. population over the age of 65, and carries with it an annual health care cost of $226 billion (2015 estimate).
The Federation of Quebec Maple Syrup Producers does not promote an increase of sugar consumption. When choosing a sweetener for moderate use, pure maple syrup has more healthful compounds compared to some other sources of sugar.

Source:

PadillaCRT

New understanding of cellular activity can lead to future strategies for dealing with neurodegenerative diseases, say Hebrew University researchers

Interesting concepts for our doctors to apply to our damage.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=126657&CultureCode=en
A new understanding of what takes place on the cellular level during the development of neurodegenerative diseases, such as Parkinson’s, Alzheimer’s, ALS and Huntington’s diseases, offers promise towards possible new strategies for combating such diseases, say Hebrew University of Jerusalem researchers.
Neurodegenerative conditions result from an impairment of motor function or cognitive function or both. This impairment results from degeneration in the particular area of the brain responsible for those functions.       
Although these neurodegenerative diseases have been functionally linked to toxic protein aggregation (deposits), there is much that is unknown about the mechanism through which aggregation causes toxicity and death at the cellular level. Inclusion bodies – structures comprised of pathogenic protein aggregates -- have long been seen as a hallmark of disease, but the relationship between inclusions and disease has remained somewhat mysterious.           
In a study published in PNAS (Proceedings of the National Academy of Sciences in the US). Hebrew University researchers (working in the lab of Dr. Daniel Kaganovich in the Cell and Developmental Biology Department, together with collaborators) present evidence that suggests that these inclusion bodies, which have traditionally been thought to accompany disease onset,actually have a cell-biological function that is not necessarily related to the disease conditions.
Further, the researchers suggest that some of those inclusion bodies not only are not toxic, but actually are part of a natural protective process. The researchers have identified two inclusion bodies, which they call JUNQ and IPOD. Aggregation in the JUNQ can lead to toxicity, whereas aggregation in the IPOD is protective.
These findings, say the Hebrew University researchers, point up a new potential strategy for designing therapeutics for neurodegenerative disease. Instead of preventing proteins from aggregating, which can be very difficult, it may be possible to enhance the cellular ability to actively enclose harmful aggregates within protective inclusions, thereby neutralizing the toxic proteins that bring on further neurodegenerative damage and even death.