Anyone who has had experience with Alzheimer's disease knows the agony of watching someone fade away as it steals memory and at the end – a person's own identity. Tonight – we'll show you an experimental way to try and beat back Alzheimer's. It's been tested on just a handful of patients – but it caught our attention because of the doctor involved, Dr. Ali Rezai, who 60 Minutes first met 20 years ago. Dr. Rezai is a neuroscience pioneer who has developed treatments for Parkinson's disease and other brain disorders. Over the last year we followed this master of the mind as he attempted to delay the progression of Alzheimer's disease and its worst symptoms using ultrasound. We saw a cutting-edge approach to brain surgery…with no cutting.
Dr. Ali Rezai: If we can, we should not be doing brain surgery.
Sharyn Alfonsi: You're a brain surgeon!
Dr. Ali Rezai: I am, but I should be out of a job, because brain surgery, it's cutting the skin, opening the skull. It can be barbaric.
A ribbon of brain tissue called cortical gray matter grows thinner in people who go on to develop dementia, and this appears to be an accurate biomarker of the disease five to 10 years before symptoms appear, researchers from The University of Texas Health Science Center at San Antonio (also called UT Health San Antonio) report.
The researchers, working with colleagues from The University of California, Davis, and Boston University, conducted an MRI brain imaging study published in Alzheimer's & Dementia. They studied 1,000 Massachusetts participants in the Framingham Heart Study and 500 people from a California cohort. The California volunteers included 44% representation of Black and Hispanic participants, whereas the Massachusetts cohort was predominantly non-Hispanic white. Both cohorts were 70 to 74 years of age on average at the time of MRI studies.
"The big interest in this paper is that if we can replicate it in additional samples, cortical gray matter thickness will be a marker we can use to identify people at high risk of dementia," said study lead author Claudia Satizabal, Ph.D., of UT Health San Antonio's Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases. "By detecting the disease early, we are in a better time window for therapeutic interventions and lifestyle modifications, and to do better tracking of brain health to decrease individuals' progression to dementia."
New Blood Test Identifies Alzheimer’s With 97% Accuracy
Though it’s still in the research phase, such a high level of accuracy brings the test one step closer to replacing expensive brain scans and spinal taps.
By Adrianna Nine January 23, 2024
Today, people who suspect they have Alzheimer’s disease tend to undergo invasive, uncomfortable, and costly brain scans or spinal taps before they receive a diagnosis. By then, symptoms have already begun to surface, offering them and their families less time to make necessary healthcare and lifestyle adjustments. But what if doctors could spot Alzheimer’s in patients before they begin to experience memory loss?
That’s the idea behind a new blood test made by ALZpath, a California-based medical diagnostics company. Called the ALZpath pTau217 assay, the test is currently available exclusively to research entities, who are busy verifying the test’s efficacy with people at risk of developing Alzheimer’s. In a study examining the results of three Alzheimer’s study cohorts, researchers at Sweden’s University of Gothenburg found that the pTau217 assay is highly accurate and could be ready for clinical research soon.
Alzheimer’s can pass between humans in rare medical accidents, suggests study
Mon 29 Jan 2024 16.00 GMT
Alzheimer’s can be spread from human to human through rare medical accidents, research suggests, although experts stress there is no evidence the disease can be passed between people through everyday activities or routine care.
Researchers say a handful of people who received human growth hormone from the pituitary glands of deceased donors have gone on to develop early onset Alzheimer’s – likely because the hormones used were contaminated with proteins that seeded the disease in their brains.
“We’re not suggesting for a moment you can catch Alzheimer’s disease. This is not transmissible in the sense of a viral or bacterial infection,” said Prof John Collinge, co-author of the study and director of the MRC Prion Unit.
“It’s only when people have been accidentally inoculated, essentially, with human tissue or extracts of human tissue containing these seeds, which is thankfully a very rare and unusual circumstance.”
The team say the new work adds weight to the idea that Alzheimer’s has similarities with prion diseases, including in the mechanism by which the proteins involved spread across the brain.
GLP-1 weight-loss drugs may pivot to treat Alzheimer's and Parkinson's
By Bronwyn Thompson
February 01, 2024
In yet another surprise attribute of the new class of obesity drugs, scientists have found that GLP-1 receptor agonists can also subdue brain inflammation, giving them a potential ‘superpower’ in the fight against Alzheimer’s and Parkinson’s diseases.
Inflammation, which is highly prevalent in those with chronic metabolic diseases, is one of the hallmarks of both Alzheimer’s and Parkinson’s.
“One of the really interesting things about the GLP-1 drugs is that beyond the control of blood sugar and body weight, they also seem to reduce the complications of chronic metabolic disease,” said study co-author Daniel Drucker, a professor in the department of medicine at the University of Toronto. “We know from clinical studies that GLP-1 does all this amazing stuff in people, but we don’t fully know how it works.”
New research suggests healthy lifestyles can help stave off dementia, perhaps by building a resilient 'cognitive reserve' in the aging brain.
The study was based on the brain autopsies on 586 people who lived to an average age of almost 91. Researchers compared each person's lifestyle and end-of-life mental skills to their neurological signs of dementia, such as brain protein plaques or changes in brain blood flow.
None of these brain factors seemed to greatly affect the positive connection between healthy living and a person's end-of-live mental skills, said a team led by Dr. Klodian Dhana, of Rush University Medical Center in Chicago.
That means that good nutrition, regular exercise and other factors may instead "provide a cognitive reserve" that buffers against negative changes going on within the brain—allowing older folk to "maintain cognitive abilities" over time, the researchers said.
Phosphodiesterase type 5 inhibitors such as Viagra are, of course, best known for effectively treating erectile dysfunction, but a study of nearly 270,000 men has added to the growing body of evidence that they may also lower the risk of developing Alzheimer's disease.
University College London (UCL) researchers looked at 269,725 male participants in the UK, with an average age of 59, with no evidence of cognitive impairment, who had recently been diagnosed with erectile dysfunction. In the five-year study, the researchers assessed the cohort in two groups: those who had prescriptions for erectile dysfunction drugs such as sildenafil (Viagra) (55% of participants), and those who did not have their erectile dysfunction treated in this way (45%).
What they found was that of the 1,119 participants who developed Alzheimer’s disease, 749 were taking erectile dysfunction drugs, while 370 were not. But when measured by person-years (the number of people in the study and the amount of time each person spent in the study), the researchers found that Alzheimer's prevalence in those on medication was 8.1 cases per 10,000 person-years, compared to 9.7 cases per 10,000 person-years for those not taking erectile dysfunction drugs.
Once they enter the body, drugs, apart from carrying out their therapeutic function, are biochemically transformed by the action of the metabolic machinery, a process that facilitates their expulsion. This biotransformation results in a gradual disappearance of the drug, which is converted into its metabolites.
These, in turn, can reach high concentrations in the body and also show a biological activity that may be different from that of the original drug. That is, the metabolites and the drug coexist in the body and can cause effects different from those obtained with the individual molecules.
This is the case of Rucaparib, a drug used in chemotherapy for ovarian cancer, breast cancer, and, more recently, prostate cancer, and its metabolite, the M324 molecule. Rucaparib is part of a group of drugs designed to treat several types of cancers that show alterations in DNA repair. Specifically, they are inhibitors of the PARP1 enzyme, involved precisely in the process of repairing mutations in the genetic material.
Phase 2 clinical trials using orally administered gold nanocrystals to treat multiple sclerosis and Parkinson’s disease have produced promising results, restoring metabolites linked to crucial energy activity in the brain that are depleted in these neurodegenerative conditions.
The brain depends on a continuous supply of energy in the form of adenosine triphosphate (ATP) to fuel its resting and active-state functions. Essential to ATP production is the molecule nicotinamide adenine dinucleotide (NAD+).
As glucose is broken down into smaller molecules by the cells, the chemical bonds holding it together break. The energy held in the broken bonds is harnessed when an electron freed during the process is captured by NAD+, converting it to its reduced form, nicotinamide adenine dinucleotide + hydrogen (NADH). NADH donates the electron to the mitochondria, which use the electron’s energy to produce ATP, a process that oxidizes NADH back to NAD+.
Infection with the virus that’s the main cause of cold sores may double a person’s risk of developing dementia, according to a new study. Adding to growing evidence of a link between the two, further research is needed to investigate whether anti-herpes treatment reduces the risk and may open the door to developing new vaccines.
Herpes simplex virus (HSV) is a common, lifelong infection that’s treatable but not curable. It’s estimated that, globally, around 67% of people under 50 have herpes simplex virus type 1 (HSV-1) infection, the main cause of oral herpes or cold sores, and around 13% have herpes simplex virus type 2 (HSV-2) infection, the main cause of genital herpes.
Another prevalent condition, dementia, is on the rise, with worldwide cases expected to reach 78 million in 2030. Although the exact cause of Alzheimer’s disease (AD), the most common form of dementia, is not yet known, growing evidence from large population-based studies has suggested that HSV infection plays a role in the development of AD or dementia. Now, a new study by researchers at Uppsala University in Sweden has examined the link between HSV infection and dementia risk.
Weizmann Institute scientists have discovered two small molecules that can cross the blood-brain barrier in mice, slowing and even reversing the effects of Huntington's, which is incurable.
The human brain is a well-guarded control center. Its system of blood vessels is surrounded by a densely packed cellular barrier that prevents most substances from getting in or out. This fortified architecture protects the brain, but it can also stop it from getting help when it needs it—for example, in the case of a neurodegenerative disease.
In a new study, published in EMBO Molecular Medicine, Prof. Rivka Dikstein of the Weizmann Institute of Science and her team identified two small molecules that manage to penetrate the blood-brain barrier and reduce the levels of a defective protein that causes Huntington's disease, an incurable neurodegenerative disorder. The new drugs not only slowed the progress of the disease in mouse models but even reversed some of its symptoms.
The signs and symptoms of Huntington's disease—slight involuntary movements, general clumsiness and increased anxiety—most commonly emerge around the age of 40. The disease develops over time and inevitably leads to death. It is caused by an excessive repetition, 36 times or more, of a DNA segment in the huntingtin gene.
Navigating Cognitive Decline: Curved Walking and Depth Cameras Unveil Early Signs
MARCH 12, 2024
First-of-its-kind study finds more gait impairments in older adults by ‘throwing them a curve’.
A first-of-its-kind study suggests that to detect subtle gait impairments in older adults that often are prevalent in the early stages of cognitive decline, “throw them a curve.”
Gait analysis, examining the way an individual stands and walks, is emerging as a valuable, non-invasive complement to cognitive assessments that aid in early diagnosis and management. In clinical settings, gait and balance tests typically focus on a straight walking path.
Exploring Curved Path Walking
This new study ventures into a different realm – curved path walking – a more natural yet complex activity. Straight walking is a rhythmic and simpler activity, whereas walking on a curving path requires greater cognitive and motor skills such as a transition time to change directions and correct balance.
College of Engineering and Computer Science researchers at Florida Atlantic University are the first to quantitatively compare the performance of healthy older adults versus older adults with mild cognitive impairment (MCI) in straight and curve walking. MCI is the early stage of cognitive decline and people with MCI have a much higher risk of transitioning to Alzheimer’s disease (AD).
Microbes stomp daffodils in creating valuable anti-Alzheimer's drug
By Michael Franco
March 15, 2024
https://newatlas.com/medical/microbes-a ... mers-drug/
Using an AI-based approach, researchers found a better way to create the drug galantamine, commonly prescribed to people suffering from Alzheimer's and other forms of dementia. The fermentation-based technique could boost the drug's availability.
While bacteria are perhaps most famous for causing diseases like strep throat and pneumonia, the tiny microbes can also be programmed to serve as the workhorses in chemical processes. For example, we've seen the probiotic Lactobacillus reuteri genetically engineered to secrete a rheumatoid arthritis drug in the body, and a modified strain of E.coli Nissle 1917 used to produce the anti-Parkinson's Disease drug L-DOPA.
Now, a team of researchers from the University of Texas (UT) has called upon E. Coli once again, this time to produce the anti-dementia drug galantamine. Galantamine works by slowing the breakdown of acetylcholine in the brain, which is an important neurotransmitter that is often degraded in the face of Alzheimer's disease and other cases of dementia. The active ingredient in galantamine is typically extracted from daffodils but that production method is time consuming and subject to the challenges faced by growing and harvesting any crop.
A team of neurologists, stem cell specialists and molecular biologists affiliated with several institutions in the U.S. and led by a group at Stanford University School of Medicine has found evidence that the root cause of Alzheimer's disease may be fat buildup in brain cells. The study is published in the journal Nature.
Prior research has suggested that Alzheimer's disease is caused by a buildup of beta-amyloid in plaques that grow between nerve cells. Other work has also implicated a protein called tau, which can build up in brain cells. Thus, most work involved in developing ways to prevent, slow or stop the disease is based on reducing or eliminating such buildups. But as the researchers with this new effort have found, there may be something else at the root of the development of the disease.
Back when Alzheimer's disease was first identified by Alois Alzheimer, he noted that in addition to the plaques and tau buildup, there was also a buildup of fat droplets in brain cells. Since that time, little effort has been made to determine whether they might be the cause of the disease.
In a paper published in the Journal of the American Medical Association (JAMA), neurologists at Beth Israel Deaconess Medical Center (BIDMC) showed that a simple skin biopsy test detects an abnormal form of alpha-synuclein, the pathological hallmark of Parkinson's disease and the subgroup of neurodegenerative disorders known as synucleinopathies, at high positivity rates.
Results from this landmark study validate this cutaneous method as a reliable and convenient tool to help physicians make more accurate diagnoses for patients and support future clinical trials for investigational drugs targeting alpha-synuclein.
A team of neurologists, stem cell specialists and molecular biologists affiliated with several institutions in the U.S. and led by a group at Stanford University School of Medicine has found evidence that the root cause of Alzheimer's disease may be fat buildup in brain cells. The study is published in the journal Nature.
Prior research has suggested that Alzheimer's disease is caused by a buildup of beta-amyloid in plaques that grow between nerve cells. Other work has also implicated a protein called tau, which can build up in brain cells. Thus, most work involved in developing ways to prevent, slow or stop the disease is based on reducing or eliminating such buildups. But as the researchers with this new effort have found, there may be something else at the root of the development of the disease.
Back when Alzheimer's disease was first identified by Alois Alzheimer, he noted that in addition to the plaques and tau buildup, there was also a buildup of fat droplets in brain cells. Since that time, little effort has been made to determine whether they might be the cause of the disease.
I'm just wondering why no one investigated this earlier?
The survival of neurons, unlike most other cells in the body, depends largely on the energy provided by mitochondria, intracellular organelles that contain their DNA to function properly.
The presence of mitochondrial DNA with deletions—the loss of fragments of DNA sequence—in cerebrospinal fluid could be an early marker of severe brain disease and an initial link in the whole neurodegenerative process, leading to the motor and cognitive symptoms associated with these disorders.
This is one of the main conclusions of the article published in the journal eBioMedicine.
The team was led by Álex Iranzo, professor at the Faculty of Medicine and Health Sciences of the University of Barcelona and director of the UB-AdSalutem Chair on Sleep and its Disorders, head of the Neurology Service of the Hospital Clinic of Barcelona, and of the clinical neurophysiology research group of the August Pi i Sunyer Biomedical Research Institute (IDIBAPS), and Ramon Trullàs, researcher of the Spanish National Research Council at the Barcelona Biomedical Research Institute (IIBB-CSIC); both linked to the Center for Biomedical Research Network in Neurodegenerative Diseases (CIBERNED).
Beyond plaques: New Alzheimer's treatment pathway discovered
By Michael Franco
March 27, 2024
https://newatlas.com/medical/pde4b-alzh ... t-pathway/
Researchers have discovered that limiting a certain enzyme can have a dramatic impact in protecting against the effects of Alzheimer's disease. The finding could lead to a new class of drugs that fight the disease.
Much of the historical research into Alzheimer's disease has focused on plaques that form in the brain thanks to the accumulation of too much amyloid proteins. Recently, though, scientists have begun looking beyond the role of these proteins (which one study suggests may form in the liver) into other probable causes of the disease and its advancement. That's largely because amyloid-based plaques, while certainly a hallmark of the disease, don't seem to be a direct cause of it, as evidenced by the failure of drugs that try to target them.
In seeking another way forward, researchers at the University of Leeds (UL) and Lancaster University (LU) in the UK, turned to an Australian study that showed that having the gene for the production of an enzyme known as PDE4B was identified as a risk factor for developing Alzheimer's.
