Category Archives: Genetic Medicine

Scientists from Cardiff University have studied the sleep patterns of children and adolescents with one of the most common genetic conditions22q11.2 deletion syndrome.

The researchers found nearly two thirds (60%) of the group aged 17 and under experienced insomnia or restless sleep and in turn, a higher proportion of these had conditions such as attention deficit hyperactivity disorder (ADHD), anxiety disorders, and conduct disorder. Whats more, those with sleep problems were also more likely to have movement problems, which can make them more clumsy and to have worse planning ability.

Children with 22q, which is also known as DiGeorge syndrome, are more likely to have poor mental health and are among those at most risk of developing psychotic disorders and schizophrenia in later life.

There are a wide range of other health issues associated with 22q, such as heart conditions and immune problems, palatal defects, speech delays, and epilepsy. It can also cause developmental and movement problems and learning disabilities.

The research has been conducted by academics involved in Cardiff Universitys ECHO Study, which furthers knowledge of genetic conditions.

Marianne van den Bree, a professor based in the School of Medicine, who leads the ECHO Study, says in a release, Parents are often concerned about the sleep problems of their child with 22q. This is the first study to systematically investigate how frequently sleep problems occur in children with this condition.

Hayley Moulding, PhD, the first author on the research paper about the sleep study, says, This research also gives us a deeper understanding of the relationship between sleep and mental health for the general population. Sleep problems can increase risk of mental health problems and mental health problems can affect quality of sleep. This can lead to a vicious cycle. I hope that further research will ultimately help break this cycle and inform improved interventions.

Estimates of how many people are affected by 22q have ranged between one in 4,000 and one in 2,000 live births but the actual figure is expected to be higher than current estimations as not all individuals may be diagnosed.

Fourteen-year-old Joshua Armour, who was diagnosed with 22q as a baby, took part in the sleep study with his brother Ethan, 12. Children with 22q were studied alongside their siblings who dont have the condition.

Joshua was diagnosed with 22q within days of being born, when doctors detected a heart defect. His first operation was at the age of eight months. He has had various other health complaints during his life, which include scoliosis, where the spine twists and turns to the side.

Victoria, Joshuas mom, says sleep was also a big issue. Hes always been up a lot in the night, she says. He gets leg pains and pains in his back. He has nightmares and has trouble going to sleep initially and then finds it difficult getting back to sleep when hes woken up.

It has a massive impact. It affects what sort of day he has in school. The tiredness has an effect on me as his carer as well as the family as a whole.

Victoria, also mom to Esmae, 9, adds, Its been great taking part in the ECHO Study. Its good to feel that we are contributing to an increased understanding of 22q.

The research paper, Sleep problems and associations with psychopathology and cognition in young people with 22q11.2 deletion syndrome, is published in Psychological Medicine.

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Sleep Problems in Children with Genetic Condition Linked to Mental Health Issues, Clumsiness, Impaired Planning Ability - Sleep Review

Mei-Jiao Chen, Hong-Fu Li, Shanying Mao

Department of Neurology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

Correspondence: Shanying Mao; Hong-Fu LiDepartment of Neurology, Second Affiliated Hospital, Zhejiang University School of Medicine, 88 Jiefang Road, Hangzhou 310009, ChinaEmail shanyingm@163.com; hongfuli@zju.edu.cn

Abstract: EhlersDanlos syndrome (EDS) type IV is characterized by thin skin with visible veins, easy bruising, characteristic facial features, arterial and digestive complications, as well as rupture of the gravid uterus. It has never been previously reported that trigeminal autonomic cephalalgias (TACs) could manifest as the only initial symptom of EDS type IV. Here, we report a case of a 27-year-old man who presented atypical headache like TACs stimulated by right internal carotid artery dissection. About one month after his discharge, he suffered dissection of the right renal artery and splenic artery, in addition to partial infarction of the right kidney and spleen. Genetic testing revealed a novel splicing variant c.799-1G>A within COL3A1. He was ultimately diagnosed with EhlersDanlos syndrome type IV. This case expanded the genetic spectrum and clinical manifestation of EDS type IV and provided a significant implication for the diagnosis of EDS type IV when the initial symptom manifested as TACs, not the typical presentation of EDS type IV.

Keywords: trigeminal autonomic cephalalgias, internal carotid artery dissection, EhlersDanlos syndrome, whole exome sequencing, Sanger sequencing

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Trigeminal Autonomic Cephalalgias Manifested As The Only Initial Sympt | JPR - Dove Medical Press

MedicalResearch.com Interview with:

Christian Sell, PhDAssociate Professor of Biochemistry and Molecular BiologyDrexel University College of Medicine

MedicalResearch.com: What is the background for this study?

Response: In terms of background, the drug rapamycin targets apathway that scientists know is critical for growth and development but is also a key regulator of lifespan in many model organisms such as worms, flies, and mice. This pathway is known as the mTOR pathway. Rapamycin is already in use clinically, it is given to people who have receivedorgan transplants to prevent rejection and is also in trials to treat some forms of cancer, at very high doses.

Many studies in mice have shown that rapamycin delays aging and prevents age-related disorders such as the decline in heart function and cognitive function. Based on this work, there is a strong expectation that these results will translate into humans, but no studies have been done due to concerns regarding potential side effects of rapamycin when the drug is given orally to prevent rejection. Our previous studies have shown that a very low dose of rapamcyin can reduce the aging of human cells and improve cell growth, while the high does used for organ transplant patients actually block cell growth. We decided to test the impact of low dose rapamycin on aging in the skin because we could treat people safely. Previous studies have shown that the drug does not get into the blood stream when high doses were given topically to people with a rare genetic disorder, so we knew that the low doses used in our study would not get into the bloodstream and would be safe for the patients.

MedicalResearch.com: What are the main findings?

Response: With this in mind, we treated subjects for 8 months with a low dose of rapamycin that preserves cell growth to see if we can reduce markers of skin aging. To our surprise, the results were better than we expected. We found a significant decrease in markers of cell aging and a significant increase in proteins associated with skin integrity. In addition, the majority of subjects enjoyed a real impact on the clinical signs of aging in their skin. Importantly, as we predicted, no rapamycin got into the bloodstream of subjects in our study.

MedicalResearch.com: What should readers take away from your report?

Response: There is a real potential to improve age-related disorders with drugs like rapamycin that target cellular aging. This is very exciting but we have to be very careful to test these interventions in a safe and responsible way. We need to understand when and where we can use these types of intervention while minimizing risks. It is an exciting time in the area of aging-related research but we have allot of work ahead. I would stress that people should not just try to take rapamycin pills. The side effects are real and can be serious.

MedicalResearch.com: What recommendations do you have for future research as a result of this work?

Response: Obviously, we need to repeat the study with more subjects. Also, we need to identify specific age-related diseases that may respond to rapamycin and carefully evaluate how to use the drug to provide benefit.

Our finding that a low dose of rapamycin is sufficient to improve signs of aging suggests that we could potentially try reducing the dose of the drug to provide benefit.

Disclosures: There is a small start-up company Boinca (pronouced Bo-Inca) that is exploring the potential for the topical application of low dose rapamycin for the treatment of skin aging. Myself and my co-authors,

Drs. Chungand Lawrence will be shareholders in that start-up.

Citation:

Christina Lee Chung, Ibiyonu Lawrence, Melissa Hoffman, Dareen Elgindi, Kumar Nadhan, Manali Potnis, Annie Jin, Catlin Sershon, Rhonda Binnebose, Antonello Lorenzini, Christian Sell.Topical rapamycin reduces markers of senescence and aging in human skin: an exploratory, prospective, randomized trial.GeroScience, 2019; DOI:10.1007/s11357-019-00113-y

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Topical Organ Rejection Drug Reduced Skin Aging - MedicalResearch.com

Dublin, Nov. 26, 2019 (GLOBE NEWSWIRE) -- The "RNAi Therapeutics Market (2nd Edition), 2019 - 2030" report has been added to ResearchAndMarkets.com's offering.

The report features an extensive study of the current market landscape and future opportunities associated with RNAi therapeutics. The study also features a detailed analysis of key drivers and trends within this evolving market.

Amongst other elements, the report includes:

One of the key objectives of the report was to estimate the existing market size and the future growth potential within the RNAi therapeutics market, over the coming decade. Based on multiple parameters, such as target patient population, likely adoption rates and expected pricing, we have provided informed estimates on the financial evolution of the market for the period 2019-2030.

The report also provides details on the likely distribution of the current and forecasted opportunity across:

In order to account for future uncertainties and to add robustness to our model, we have provided three market forecast scenarios, namely conservative, base and optimistic scenarios, representing different tracks of the industry's growth.

The opinions and insights presented in this study were influenced by discussions conducted with multiple stakeholders in this domain. The report features detailed transcripts of interview(s) held with Amotz Shemi, CEO, Silenseed.

All actual figures have been sourced and analyzed from publicly available information forums and primary research discussions. Financial figures mentioned in this report are in USD, unless otherwise specified.

List of Chapters Covered

1. Preface2. Executive Summary3. Introduction4. Competitive Landscape5. Company Competitiveness Analysis6. Late Stage RNAi Therapeutics7. Technology Platforms and Delivery Systems8. Key Therapeutic Indications9. Clinical Trial Analysis10. Patent Analysis11. Recent Partnerships12. Funding and Investment Analysis13. Promotional Analysis14. Market Sizing and Opportunity Analysis15. RNAi in Diagnostics16. Service Providers for RNAi Therapeutics17. SWOT Analysis18. Conclusion19. Interview Transcript(s)20. Appendix 1: Tabulated Data21. Appendix 2: List of Companies and Organizations

Chapter Outlines

Chapter 2 is an executive summary of the key insights captured during our research. It offers a high-level view on the current state of the market for RNAi therapeutics and its likely evolution in the short-mid term to long term.

Chapter 3 provides a general overview of RNAi therapeutics, including a discussion on their historical background and mechanism. In addition, it includes information on the type of RNAi molecule, along with their mechanisms of action and application areas. Further, the chapter features a discussion on the historical evolution of the domain, advantages and associated challenges, and the views of the regulatory authorities.

Chapter 4 includes information on over 150 RNAi pipeline candidates that are currently in different stages of development. It features a detailed analysis of the pipeline molecules, highlighting phase of development, target indication(s), key therapeutic areas, type of RNAi molecule, target genes, route of administration, mechanism of action and special drug designation (if any). Further, it presents the detailed overview of therapy developers, providing information on year of establishment, location of headquarters and company size. In addition, it features a logo landscape of product developers based on location of headquarters and company size.

Chapter 5 presents a three-dimensional bubble analysis of key players engaged in this domain, evaluating respective product portfolios, type of RNAi molecule, target therapeutic area, company size and its year of establishment.

Chapter 6 contains detailed profiles of drug candidates that are in the advanced stages of development (phase II/III and above). Each profile provides information on their current status of development, mechanism of action, route of administration, affiliated technology platform (if available), dosage, clinical trial results, along with information on respective developers.

Chapter 7 provides a list of technology platforms that are either available in the market or are being designed for the targeted delivery of RNAi drugs. In addition, it features brief profiles of some of the key technologies. Each profile contains details on the various pipeline molecules that have been/are being developed using the technology and patents associated with the technology.

Chapter 8 highlights the potential target indications (segregated by therapeutic areas) that are currently the prime focus of companies developing RNAi therapeutics. These therapeutic areas include oncological disorders, infectious diseases, genetic disorders, ophthalmic diseases, respiratory disorders, hepatic disorders, metabolic disorders, cardiovascular disorders, dermatological disorders.

Chapter 9 is an analysis of completed, ongoing and planned clinical studies for different types of RNAi molecules. For the purpose of this analysis, we considered the clinical studies registered till September 2019, and analyzed them on the basis of various parameters, such as registration year, current status, phase of development, type of RNAi molecule, regional distribution of clinical trials, and enrolled patient population across different geographies.

Chapter 10 provides insights from a detailed patent analysis, presenting an overview of the filed/granted patents related to RNAi therapeutics since 2014. For this analysis, we looked at the patents that have been published by various players till March 2019. It also highlights the important information and trends associated with these patents, including patent type (granted patents, patent applications and others), patent publication year, regional distribution, CPC symbols, emerging focus areas and the leading industry/academic players (in terms of the number of patents filed/granted). The chapter also includes a patent benchmarking analysis and a detailed valuation analysis.

Chapter 11 features an elaborate analysis and discussion on the various collaborations and partnerships that have been inked amongst stakeholders in this domain, since 2014. It includes a brief description of various types of partnership models (namely mergers/acquisitions, licensing agreements, product development and commercialization agreements, R&D agreement, and other agreements) that have been adopted by stakeholders in this domain.

Chapter 12 presents details on various investments received by start-ups/small companies that are engaged in this domain. The chapter includes information on various types of investments (such as venture capital financing, debt financing, grants, capital raised from IPO and subsequent offerings) received by the companies between 2014 and 2019, highlighting the growing interest of the venture capital community and other strategic investors in this domain.

Chapter 13 highlights the key promotional strategies that are being implemented by the developers of the already marketed oligonucleotide products, namely Defitelio, EXONDYS 51 and ONPATTRO. The promotional aspects covered in the chapter include details provided on the product website (covering key messages for patients and healthcare professionals), patient support offerings and informative downloadable content.

Chapter 14 presents an informed forecast analysis, highlighting the future potential of the market, till the year 2030. It also includes future sales projections of RNAi therapeutics that are either marketed or in advanced stages of clinical development (phase II/III and above). Sales potential and growth opportunity were estimated based on the target patient population, likely adoption rates, existing/future competition from other drug classes and the likely price of products. The chapter also presents a detailed market segmentation on the basis of [A] key therapeutic areas (oncological disorders, genetic disorders, metabolic disorders, hematological disorders, ophthalmic disorders and others), [B] route of administration (subcutaneous, intravenous, topical and intradermal), [C] share of leading industry players, [D] type of RNAi molecule and [E] key geographical regions (US, Europe and Asia-Pacific).

Chapter 15 discusses the use of miRNAs as potential biomarkers and enlists several miRNA biomarkers currently under investigation. In addition, the chapter provides the pipeline of diagnostic kits that have already been approved or are under development.

Chapter 16 provides information on the companies that are actively supporting the development of RNAi therapeutics market. These include contract manufacturers, contract researcher organizations and other service providers. In addition, the chapter includes an analysis based on parameters such as type of service provider, location of their headquarters and type of RNAi molecule.

Chapter 17 provides a detailed discussion on affiliated trends, key drivers and challenges, under a comprehensive SWOT framework, featuring a Harvey ball analysis, highlighting the relative impact of each SWOT parameter on the RNAi therapeutics market.

Chapter 18 summarizes the entire report. It presents the list of key takeaways and offers our independent opinion on the current market scenario.

Chapter 19 is a collection of interview transcripts of the discussions that were held with key stakeholders in this market. The chapter provides details of interview(s) held with Amotz Shemi, CEO, Silenseed.

Chapter 20 is an appendix, which provides tabulated data and numbers for all the figures included in the report.

Chapter 21 is an appendix, which provides the list of companies and organizations mentioned in the report.

Companies Mentioned

For more information about this report visit https://www.researchandmarkets.com/r/bufa1v

Research and Markets also offers Custom Research services providing focused, comprehensive and tailored research.

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Worldwide RNAi Therapeutics Market Outlook to 2030 - More Than $5.5 Billion in Capital has Been Invested by Various Private & Public Investors to...

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School of Medicine leading multicenter study aimed at understanding brain development in babies with the condition

Kelly N. Botteron, MD, a professor of psychiatry and of radiology at Washington University School of Medicine in St. Louis, is leading a multicenter brain-imaging study focused on infants with Down syndrome. The five-year, $11.5 million grant from the National Institutes of Health (NIH) will focus on brain development in babies with the genetic syndrome.

Researchers at Washington University School of Medicine in St. Louis have received a five-year, $11.5 million grant to lead a multicenter effort to understand how brain development in babies with Down syndrome differs from that in other babies. The effort, which involves scanning the babies brains using MRI, will provide a foundation that may lead to therapies to counter developmental delays in children with the condition.

The grant, from the National Institutes of Health (NIH), is part of a $77 million initiative that began in 2018 to bolster basic and clinical research focused on infants and children with Down syndrome. Most people with the genetic condition have mild to severe developmental delays, learning disabilities, and distinct facial and physical features. Some also experience heart and gastrointestinal disorders.

Each year, about 6,000 babies in the U.S. are born with the condition.

It is astounding how sparse the research is involving neuroimaging characterization of neurodevelopment in Down syndrome, especially given that the condition is rather common, said the studys lead investigator, Kelly N. Botteron, MD, a Washington University professor of psychiatry and of radiology. Brain-imaging studies in children with Down syndrome are almost nonexistent. Before we can develop and assess therapies to improve cognitive outcomes, we need to understand more about the alterations in early brain development in these children.

Researchers will conduct behavioral and developmental testing, as well as MRI brain imaging, to examine the brain structure and cognitive function of 140 infants with Down syndrome and 70 babies without the condition. The children will be studied when they are 6 months old and, again, when they are 1 year old and then 2 years old.

The researchers also will compare the brain scans of the two groups of children with scans of autistic infants and toddlers. Such scans in autistic children have been part of a separate multicenter study co-led by Washington University.

This will give us a large set of data to detect differences in neurodevelopmental patterns, Botteron said. It will be eye-opening because there are some developmental characteristics that are unique to children with Down syndrome. They tend to have more motor and coordination delays, in addition to language delays. This information is critical to developing potential innovative treatment trials including additional physical therapy, applied behavior analyses, novel drugs and potential genetic editing techniques to improve both the quality of life and overall health of people with Down syndrome.

The infants will undergo MRI scans, generally in the evening after they fall asleep naturally, nixing the need for anesthesia. The researchers have developed strategies for scanning the brains of babies, based on MRI, without disturbing infants sleep.

Over the past 10 to 15 years, weve learned a lot about conducting brain imaging on infants and children with autism and healthy comparison controls, Botteron said.

One tactic is to introduce the babies beforehand to noise they can expect to hear from the MRI machine. Its important to prepare the babies and toddlers, she said. This means making them comfortable and scanning them at night while theyre naturally sleeping.

The studys other participants include researchers from the University of Washington in Seattle; Childrens Hospital of Philadelphia; University of North Carolina; University of Minnesota; New York University; and the Montreal Neurological Institute in Canada.

Washington University School of Medicines 1,500 faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is a leader in medical research, teaching and patient care, ranking among the top 10 medical schools in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.

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Brain imaging of babies with Down syndrome focus of $11.5 million grant - Washington University School of Medicine in St. Louis

In the 90s, Alzheimers researchers were full of optimism. New genetic studies all pointed to one culprithard clumps of protein, called amyloid, that litter the brains of people with the disease.

With the emergence of the first tangible target, pharmaceutical companies jumped in to develop drugs to clear amyloid from the brain. In animals, the drugs appeared to improve memory. But the results of human clinical trials that followed were disheartening: One after one, these drugsall designed to target amyloidhave failed to slow the disease.

The onslaught of news about these failures has left the public wondering whether amyloid has anything to do with Alzheimersand whether a new approach is needed.

The field has already begun to redirect its focus, says Scott Small, MD, director of Columbias Alzheimers Disease Research Center and theBoris and Rose Katz Professor of Neurology at Columbia University Vagelos College of Physicians and Surgeons.

Theres now reason to be cautiously optimismistic, he says, because we have uncovered new pathways that lead to the disease, and we know that they truly make a difference.

The CUIMC Newsroom spoke with Small about the current state of research into Alzheimers treatments and prevention.

In retrospect, the idea that reducing amyloid in the brainwhich all the failed drugs dois based on an incomplete picture of the disease.

To treat a disease, we need to treat whats broken. But its very difficult to find whats broken in these slowly progressive brain disorders.

One way to find whats broken is through genetics, but the first wave of genetic studies in the 80s and 90s only had the technical capabilities to investigate Alzheimers cases that run in families, those caused by a single gene.

The results of these studies all seemed to converge on one biological process: amyloid.

But these single-gene forms of Alzheimers are rareand account for maybe 2% to 3% of cases. Most cases of Alzheimers are caused by a complex interplay of many genes and the environment.

The field made the assumption that amyloid is the primary culprit in all forms of Alzheimers. It made perfect sense, because we see amyloid in all patients with Alzheimers, whether their disease is caused by a single gene or not.The amyloid finding was extremely exciting, and there was a sense that we were on the cusp of curing this devastating, horrible disease.

The amyloid hypothesis is that amyloid is the trigger of everything in Alzheimers. That seems now to be wrong.

New studies from the past decade tell us that amyloid is part of the story of Alzheimers disease, but its the smoke, not the fire. Weve learned that the single-gene and more common, complex forms of Alzheimers are not identical, though they do overlap.

Theres been a lot of backlash against the amyloid hypothesis lately, but in the 90s, it was the right idea. The pharmaceutical industry was right to jump on the amyloid bandwagon. And theyre now right to give it up, I think.

Back in the 80s and 90s, genetic tools weren't quite developed enough to address the real question we had: What genes are involved in most cases of Alzheimers disease?

Techniques have advanced and we can now answer this question. New studiesmany led by Richard Mayeux, MD[chair of neurology at Columbia]have been pointing to other processes in the brain. We also have better biological tools that can reveal the basic problem inside neurons.

Based on this research, the new consensus in the field is that there are two other pathways that cause the disease.

One involves protein trafficking, which is how proteins are shipped to different sites within a single cell. The health of neurons, more so than other cells, depends on protein trafficking in and out of one particular site: the endosome.

In Alzheimers, the flow of proteins out of the endosome is blocked, and we think that causes the other problems we see in the disease: the amyloid, the tau tangles also common in the Alzheimers brain, and the neurodegeneration. Essentially it's a plumbing problem.

Our research here at Columbia provided some early evidence for an endosomal trafficking problem in Alzheimers. And genetic studiesincluding those led by Dr.Mayeuxhave now found that some endosomal genes are linked to Alzheimers, which provides more support.

The second pathway involves microglia, which are cells in the brain that help maintain the health of neurons and help keep the spaces between neurons clear of pathogens, protein aggregates, and other cellular debris.

Recently discovered genesby Phil De Jager, MD, PhD, in our center and otherspoint us to these cells. But what exactly is wrong with the microglia is still hotly debated. We dont know if theyre working too well or not well enough, but we do know theyre not working properly.

We now, I believe, have evidence to help us understand why the first hypothesis was wrong. Scientifically, we have very good justification to argue why our new hypotheses are correct.

Were now seeing that companies are getting back into drug development because these new pathways are so compelling.

In the coming years, our biggest focus at the Alzheimers Disease Research Center at Columbia will be accelerating drug discovery. One of the most important goals is to develop new biomarkersfor the new Alzheimers pathways. These biomarkers are crucial for developing the new generation of theraputic agents.These biomarkers will be useful for enrolling patients into new anticipated clinical trials, following the logic of precision medicine.Also, just as biomarkers of amyloid were important for testing assumptions about the primacyof amyloid in the disease, these biomarkers are important for testingor potentially refutingthe new pathways.

Were also testing gene therapies and other ways to restore endosomal traffickingto see if that prevents neurodegeneration in animal models.

Frank Provenzano and Adam Brickman are developing new techniques, with imaging and cognitive testing, to detect patients with endosomal defects as early as possible. We think the sooner we can treat people, the better. Sabrina Simoes, one of our newest members, is developing new ways to use spinal fluid and blood to remotely monitor endosomal trafficking. Thats a critical step in measuring a drugs effectiveness when the drug moves to clinical testing.

In science, though, you never can be sure.The only way well know were right is by developing drugs and testing the hypothesis in clinical trials in patients, like we did with the amyloid hypothesis.

In my practice, I encounter many people who have family members with Alzheimer's and theyre worried about that their genes. But in most cases, just because your mother has it, doesnt mean youre going to get it.

In a complex disease, each gene and each environmental factor is like putting a pebble on a scale. None of them by themselves can prevent or cause Alzheimers.So if your parent has Alzheimers, that puts one pebble on the scale. But if you went to college, if you exercise, those are pebbles on the other side of the scale.

Many of the things that we thought historically cause Alzheimer's have been debunkedfor example, the idea that itwas caused by various heavy metals. But we do know that maintaining cardiac health is good: Exercise is good; smoking is bad; developing diabetes or obesity increases the risk.These recommendations, as most people know, are true for any disease.

People often ask me this question, hoping I know something that no one else does. I dont have any other answers at the moment, but everyone in the field is doing their best to find new ways to forestall this disease.

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Will a Treatment for Alzheimer's Ever Be Found? - Columbia University Irving Medical Center