Sam Gandy

Last updated
Sam Gandy
NationalityAmerican
Education
B.S., Charleston Southern University (Chemistry)

M.D., Ph.D., Medical University of South Carolina (Molecular Cell Biology)

Columbia University College of Physicians and Surgeons

Cornell University Medical College

The Rockefeller University
Nathan S. Kline Institute for Psychiatric Research

Years active1986-present
Medical career
ProfessionPhysician, Scientist
Institutions
Mount Sinai

South Australia Health and Medical Research Institute

Rockefeller University
New York Hospital Cornell Medical Center
ResearchAmyloid impact in Alzheimer’s disease, neurology, cell biology

Samuel E. Gandy, is a neurologist, cell biologist, Alzheimer's disease (AD) researcher and expert in the metabolism of the sticky substance called amyloid that clogs the brain in patients with Alzheimer's. His team discovered the first drugs that could lower the formation of amyloid. [1]

Contents

As of 2020, he is Mount Sinai Professor of Alzheimer's Disease Research, [2] professor of neurology and psychiatry, Icahn School of Medicine at Mount Sinai, [3] director, Center for Cognitive Health and NFL Neurological Center Mount Sinai Hospital, [4] visiting principal research fellow, South Australia Health and Medical Research Institute in Adelaide, SA, Australia, and chairman emeritus of the National Medical and Scientific Advisory Council of the Alzheimer's Association. He was also founding director, Farber Institute for the Neurosciences. [1] [5] [6]

Research

Gandy has written more than 250 peer-reviewed papers, [7] chapters and reviews on this topic. He has received continuous National Institutes of Health (NIH) funding for his research on amyloid metabolism since 1986. [8] He holds four patents that can be implemented to regulate key proteins, inhibiting Alzheimer-type amyloidosis and a diagnostic method for Alzheimer disease, Huntington's disease, Parkinson's disease, dystonia ataxia, schizophrenia, epilepsy, brain tumors, brain irradiation, head trauma, and acute and chronic encephalitic and vascular disease. Gandy also studies brain imaging as a tool to confirm chronic traumatic encephalopathy (CTE) in retired athletes and war Veterans during their lifetimes. [9]

Patents

Grants

Gandy worked on 36 research grants, 18 as principal investigator, since 1986. As of 2020, he works on nine active grants. [14] [15] [16] [17] [18]

Partial list of active grants in 2020:

Funding Source, & NumberProject TitleDescription
NIH-NIA to NYSCF, R01 AG061894Use of iPSC systems to define roles of microglial TREM2/DAP12 and CR3/DAP12 complexes and their genetic variants in specifying risk for late-onset sporadic Alzheimer’s disease.Develop a system based on mixing various individual iPSC-derived brain cell types or on the cultivation of organoids where all the cell types are naturally represented.
NIH-NIA, U01 AG046170Integrative Network Biology Approaches to Identify, Characterize and Validate Molecular Subtypes in AD.Identify and characterize molecular subtypes of AD with state-of-the-art network biology approaches to all existing large-scale genetic, gene expression, proteomic and functional MRI data
NIH-NIA, R01AG058469Integrated understanding of complex viral network biology in Alzheimer’s DiseaseDevelop and experimentally evaluate novel molecular models of microbial perturbation in AD.
NIH-NIA, RF1AG059319Systematic Drug Repurposing Targeting Immune Activation Networks in Alzheimer’s DiseaseTo leverage recent insights from genetic studies and drug repurposing to identify established therapies that could be repurposed to meet the great unmet need for new and effective treatments targeting immune dysfunction in AD.
NIH, R01AG057907Integrative Network Modeling of Cognitive Resilience to Alzheimer’s DiseaseSystematically develop and validate molecular network models underlying cognitive resilience to AD risk.

Editorialships and boards

As of 2020, Gandy is on the editorial boards of Neurodegenerative Diseases , Journal of Neuroinflammation and The Journal of Biological Chemistry. He is an associate editor at Alzheimer’s Disease and Associated Disorders and Journal of Neuroinflammation. [19] [20]

Publications

Gandy has an h-index of 83 [21] in 2020; a partial list of peer-reviewed publications include:

Biography

Gandy received his MD and PhD at the Medical University of South Carolina. [22]

He did his postgraduate work at the Columbia University College of Physicians & Surgeons and Cornell University Medical College. Gandy completed his post-doctorate at Rockefeller University, where he was appointed assistant professor in the laboratory of Paul Greengard, 2000 Laureate of the Nobel Prize in Physiology or Medicine. [1] [19]

Gandy was appointed associate professor of neurology and neurosciences at Cornell University Medical College in 1992. In 1997, he moved to New York University where he served as professor of psychiatry and cell biology until his appointment as Paul C. Brucker, M.D., Professor of Neuroscience at Jefferson Medical College and Director of the Farber Institute for Neurosciences in 2001. In July 2007, he assumed his current post as Sinai Professor of Alzheimer’s Disease Research at the Mount Sinai School of Medicine. He is also a member of the Research Consortium of the Cure Alzheimer's Fund. [23]

In 2009, Gandy was featured with other prominent research scientists as one of GQ's "Rockstars of Science" [24] and featured in the documentary film I Remember Better When I Paint that examines the phenomenon of how the creative arts awaken pathways to emotional parts of the brain. [25]

Related Research Articles

Vascular dementia (VaD) is dementia caused by problems in the blood supply to the brain, resulting from a cerebrovascular disease. Restricted blood supply (ischemia) leads to cell and tissue death in the affected region, known as an infarct. The three types of vascular dementia are subcortical vascular dementia, multi-infarct dementia, and stroke related dementia. Subcortical vascular dementia is brought about by damage to the small blood vessels in the brain. Multi-infarct dementia is brought about by a series of mini-strokes where many regions have been affected. The third type is stroke related where more serious damage may result. Such damage leads to varying levels of cognitive decline. When caused by mini-strokes, the decline in cognition is gradual. When due to a stroke, the cognitive decline can be traced back to the event.

<span class="mw-page-title-main">Amyloid plaques</span> Extracellular deposits of the amyloid beta protein

Amyloid plaques are extracellular deposits of the amyloid beta (Aβ) protein mainly in the grey matter of the brain. Degenerative neuronal elements and an abundance of microglia and astrocytes can be associated with amyloid plaques. Some plaques occur in the brain as a result of aging, but large numbers of plaques and neurofibrillary tangles are characteristic features of Alzheimer's disease. Abnormal neurites in amyloid plaques are tortuous, often swollen axons and dendrites. The neurites contain a variety of organelles and cellular debris, and many of them include characteristic paired helical filaments, the ultrastructural component of neurofibrillary tangles. The plaques are highly variable in shape and size; in tissue sections immunostained for Aβ, they comprise a log-normal size distribution curve with an average plaque area of 400-450 square micrometers (µm²). The smallest plaques, which often consist of diffuse deposits of Aβ, are particularly numerous. The apparent size of plaques is influenced by the type of stain used to detect them, and by the plane through which they are sectioned for analysis under the microscope. Plaques form when Aβ misfolds and aggregates into oligomers and longer polymers, the latter of which are characteristic of amyloid. Misfolded and aggregated Aβ is thought to be neurotoxic, especially in its oligomeric state.

<span class="mw-page-title-main">Cerebral amyloid angiopathy</span> Disease of blood vessels of the brain

Cerebral amyloid angiopathy (CAA) is a form of angiopathy in which amyloid beta peptide deposits in the walls of small to medium blood vessels of the central nervous system and meninges. The term congophilic is sometimes used because the presence of the abnormal aggregations of amyloid can be demonstrated by microscopic examination of brain tissue after staining with Congo red. The amyloid material is only found in the brain and as such the disease is not related to other forms of amyloidosis.

<span class="mw-page-title-main">Neurofibrillary tangle</span> Aggregates of tau protein known as a biomarker of Alzheimers disease

Neurofibrillary tangles (NFTs) are aggregates of hyperphosphorylated tau protein that are most commonly known as a primary biomarker of Alzheimer's disease. Their presence is also found in numerous other diseases known as tauopathies. Little is known about their exact relationship to the different pathologies.

Pittsburgh compound B (PiB) is a radioactive analog of thioflavin T, which can be used in positron emission tomography scans to image beta-amyloid plaques in neuronal tissue. Due to this property, Pittsburgh compound B may be used in investigational studies of Alzheimer's disease.

<span class="mw-page-title-main">Tauopathy</span> Medical condition

Tauopathy belongs to a class of neurodegenerative diseases involving the aggregation of tau protein into neurofibrillary or gliofibrillary tangles in the human brain. Tangles are formed by hyperphosphorylation of the microtubule protein known as tau, causing the protein to dissociate from microtubules and form insoluble aggregates. The mechanism of tangle formation is not well understood, and whether tangles are a primary cause of Alzheimer's disease or play a peripheral role is unknown.

<span class="mw-page-title-main">Neurodegenerative disease</span> Central nervous system disease

A neurodegenerative disease is caused by the progressive loss of structure or function of neurons, in the process known as neurodegeneration. Such neuronal damage may ultimately involve cell death. Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, multiple system atrophy, and prion diseases. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable; however research has shown that the two major contributing factors to neurodegeneration are oxidative stress and inflammation. Biomedical research has revealed many similarities between these diseases at the subcellular level, including atypical protein assemblies and induced cell death. These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well.

<span class="mw-page-title-main">Chronic traumatic encephalopathy</span> Neurodegenerative disease caused by head injury

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease linked to repeated trauma to the head. The encephalopathy symptoms can include behavioral problems, mood problems, and problems with thinking. The disease often gets worse over time and can result in dementia.

<span class="mw-page-title-main">Proteinopathy</span> Medical condition

In medicine, proteinopathy, or proteopathy, protein conformational disorder, or protein misfolding disease, is a class of diseases in which certain proteins become structurally abnormal, and thereby disrupt the function of cells, tissues and organs of the body. Often the proteins fail to fold into their normal configuration; in this misfolded state, the proteins can become toxic in some way or they can lose their normal function. The proteinopathies include such diseases as Creutzfeldt–Jakob disease and other prion diseases, Alzheimer's disease, Parkinson's disease, amyloidosis, multiple system atrophy, and a wide range of other disorders. The term proteopathy was first proposed in 2000 by Lary Walker and Harry LeVine.

The prevention of dementia involves reducing the number of risk factors for the development of dementia, and is a global health priority needing a global response. Initiatives include the establishment of the International Research Network on Dementia Prevention (IRNDP) which aims to link researchers in this field globally, and the establishment of the Global Dementia Observatory a web-based data knowledge and exchange platform, which will collate and disseminate key dementia data from members states. Although there is no cure for dementia, it is well established that modifiable risk factors influence both the likelihood of developing dementia and the age at which it is developed. Dementia can be prevented by reducing the risk factors for vascular disease such as diabetes, high blood pressure, obesity, smoking, physical inactivity and depression. A study concluded that more than a third of dementia cases are theoretically preventable. Among older adults both an unfavorable lifestyle and high genetic risk are independently associated with higher dementia risk. A favorable lifestyle is associated with a lower dementia risk, regardless of genetic risk. In 2020, a study identified 12 modifiable lifestyle factors, and the early treatment of acquired hearing loss was estimated as the most significant of these factors, potentially preventing up to 9% of dementia cases.

<span class="mw-page-title-main">Alzheimer's disease</span> Progressive neurodegenerative disease

Alzheimer's disease (AD) is a neurodegenerative disease that usually starts slowly and progressively worsens, and is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation, mood swings, loss of motivation, self-neglect, and behavioral issues. As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the typical life expectancy following diagnosis is three to nine years.

Early-onset Alzheimer's disease (EOAD), also called Younger-onset Alzheimer's disease (YOAD), is Alzheimer's disease diagnosed before the age of 65. It is an uncommon form of Alzheimer's, accounting for only 5–10% of all Alzheimer's cases. About 60% have a positive family history of Alzheimer's and 13% of them are inherited in an autosomal dominant manner. Most cases of early-onset Alzheimer's share the same traits as the "late-onset" form and are not caused by known genetic mutations. Little is understood about how it starts.

Alzheimer's Disease Neuroimaging Initiative (ADNI) is a multisite study that aims to improve clinical trials for the prevention and treatment of Alzheimer's disease (AD). This cooperative study combines expertise and funding from the private and public sector to study subjects with AD, as well as those who may develop AD and controls with no signs of cognitive impairment. Researchers at 63 sites in the US and Canada track the progression of AD in the human brain with neuroimaging, biochemical, and genetic biological markers. This knowledge helps to find better clinical trials for the prevention and treatment of AD. ADNI has made a global impact, firstly by developing a set of standardized protocols to allow the comparison of results from multiple centers, and secondly by its data-sharing policy which makes available all at the data without embargo to qualified researchers worldwide. To date, over 1000 scientific publications have used ADNI data. A number of other initiatives related to AD and other diseases have been designed and implemented using ADNI as a model. ADNI has been running since 2004 and is currently funded until 2021.

Florbetaben, a fluorine-18 (18F)-labeled stilbene derivative, trade name NeuraCeq, is a diagnostic radiotracer developed for routine clinical application to visualize β-amyloid plaques in the brain. It is indicated for Positron Emission Tomography (PET) imaging of β-amyloid neuritic plaque density in the brains of adult patients with cognitive impairment who are being evaluated for Alzheimer's disease (AD) and other causes of cognitive impairment. β-amyloid is a key neuropathological hallmark of AD, so markers of β-amyloid plaque accumulation in the brain are useful in distinguishing AD from other causes of dementia. The tracer successfully completed a global multicenter phase 0–III development program and obtained approval in Europe, US and South Korea in 2014.

<span class="mw-page-title-main">Giulio Maria Pasinetti</span>

Giulio Maria Pasinetti is the Program Director of the Center on Molecular Integrative Neuroresilience and is the Saunders Family Chair in Neurology at the Icahn School of Medicine at Mount Sinai (ISMMS) in New York City. Pasinetti is a Professor of Neurology, Psychiatry, Neuroscience, and Geriatrics and Palliative Medicine at ISMMS.

The neuroscience of aging is the study of the changes in the nervous system that occur with ageing. Aging is associated with many changes in the central nervous system, such as mild atrophy of the cortex that is considered non-pathological. Aging is also associated with many neurological and neurodegenerative disease such as amyotrophic lateral sclerosis, dementia, mild cognitive impairment, Parkinson's disease, and Creutzfeldt–Jakob disease.

Parkinson's disease dementia (PDD) is dementia that is associated with Parkinson's disease (PD). Together with dementia with Lewy bodies (DLB), it is one of the Lewy body dementias characterized by abnormal deposits of Lewy bodies in the brain.

Mathias Jucker is a Swiss neuroscientist, Professor, and a Director at the Hertie Institute for Clinical Brain Research of the University of Tübingen. He is also a group leader at the German Center for Neurodegenerative Diseases in Tübingen. Jucker is known for his research on the basic biologic mechanisms underlying brain aging and Alzheimer’s disease.

Alzheimer's disease (AD) in African Americans is becoming a rising topic of interest in AD care, support, and scientific research, as African Americans are disproportionately affected by AD. Recent research on AD has shown that there are clear disparities in the disease among racial groups, with higher prevalence and incidence in African Americans than the overall average. Pathologies for Alzheimer’s also seem to manifest differently in African Americans, including with neuroinflammation markers, cognitive decline, and biomarkers. Although there are genetic risk factors for Alzheimer’s, these account for few cases in all racial groups.

Donald F. Weaver MD, PhD is a Canadian chemist and neurologist based at the Krembil Research Institute, University Health Network, University of Toronto, Canada. He is currently Senior Scientist of the Krembil Research Institute and Professor of Neurology, Chemistry, and Pharmaceutical Sciences, University of Toronto. He is a Fellow of the Royal College of Physicians (Canada), Fellow of the Chemical Institute of Canada, and Fellow of the Canadian Academy of Health Sciences.

References

  1. 1 2 3 "Sam Gandy". Cure Alzheimer's Fund. Retrieved 2020-01-22.
  2. ↑ Kaiser, Jocelyn (30 August 2018). "The Alzheimer's gamble: NIH tries to turn billions in new funding into treatment for deadly brain disease". Science. doi:10.1126/science.aav2455. S2CID   81526319.
  3. ↑ "Medscape Neurology Scientific Advisory Board". www.medscape.com. Retrieved 2020-01-22.
  4. ↑ "Concussions May Leave Former NFL Players With Another Issue: Impotence". Consumer HealthDay. Retrieved 2020-01-22.
  5. ↑ "Alzheimer's Disease Treatment on MedicineNet.com". MedicineNet. Retrieved 2020-01-22.
  6. ↑ Australia, Dementia (2018-06-11). "Alzheimer's Australia National Conference 2017 - Speakers". www.dementia.org.au. Retrieved 2020-01-22.
  7. ↑ "South Australian Health and Medical Research Institute | 100&Change Solutions Bank". 100 and Change. Retrieved 2020-01-22.
  8. ↑ "GQ's Rock Stars of Science".
  9. ↑ "All My Fathers : Tickets". ALL MY FATHERS. Retrieved 2020-01-22.
  10. ↑ US 4874694,Gandy, Samuel E.&Greengard, Paul,"United States Patent: 4874694 - Use of phosphoprotein patterns for diagnosis of neurological and psychiatric disorders",published 1989-10-17, assigned to The Rockefeller University
  11. ↑ US 5242932,Gandy, Samuel E.; Caporaso, Gregg L.& Greengard, Paul,"Treatment of amyloidosis associated with Alzheimer disease",published 1993-09-07, assigned to The Rockefeller University
  12. ↑ US 5348963,Gandy, Samuel E.; Caporaso, Gregg L& Greengard., Paul,"Method of screening for modulators of amyloid formation",published 1994-09-20, assigned to The Rockefeller University
  13. ↑ US 5385915,Buxbaum, Joseph D.; Gandy, Samuel E.& Greengard, Paul,"Treatment of amyloidosis associated with Alzheimer disease using modulators of protein phosphorylation",published 1995-01-31, assigned to The Rockefeller University
  14. ↑ Fossati, Valentina; Gandy, Samuel; Noggle, Scott. "Use of iPSC systems to define roles of microglial TREM2/DAP12 and CR3/DAP12 complexes and their genetic variants in specifying risk for late onset sporadic Alzheimer's disease". Grantome.
  15. ↑ Ehrlich, Michelle; Gandy, Samuel; Haroutunian, Vahram; Iijima, Koichi; Noggle, Scott; Schadt, Eric; Zhang, Bin; Zhu, Jun. "Integrative Biology Approach to Complexity of Alzheimer's Disease". Grantome.
  16. ↑ "Integrated understanding of complex viral network biology in Alzheimer's Disease - Dimensions". app.dimensions.ai. Retrieved 2020-01-22.
  17. ↑ "SYSTEMATIC DRUG REPURPOSING TARGETING IMMUNE ACTIVATION NETWORKS IN ALZHEIMER'S DISEASE (AD) - Dimensions". app.dimensions.ai. Retrieved 2020-01-22.
  18. ↑ "Alzheimer's Disease Research Center - Dimensions". app.dimensions.ai. Retrieved 2020-01-22.
  19. 1 2 "Geoffrey Beene | Sam Gandy" . Retrieved 2020-01-22.
  20. ↑ "Molecular Neurodegeneration". Molecular Neurodegeneration. Retrieved 2020-01-22.
  21. ↑ "Samuel Gandy - Google Scholar". scholar.google.com. Retrieved 2020-08-28.
  22. ↑ "Mount Sinai Hospital".
  23. ↑ "Cure Alzheimer's Fund".
  24. ↑ "MedScape Today".
  25. ↑ "Alzheimer's film: I Remember Better When I Paint, Paris Writer's News". 16 December 2009.
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