Michael Geschwind

Last updated
Michael D. Geschwind
Education Albert Einstein College of Medicine (M.D., Ph.D.)

UCLA Medical Center (internship)
Johns Hopkins School of Medicine (residency)

UCSF Memory and Aging Center (fellowship)
OccupationProfessor of Neurology
Medical career
ProfessionProfessor
FieldNeurology
Institutions UCSF Memory and Aging Center
Research Neurodegenerative disorders

Michael D. Geschwind is a professor of neurology at the UCSF Memory and Aging Center (MAC), specializing in neurodegenerative disorders. [1]

Geschwind has published highly cited papers on rapidly progressive dementias, [2] [3] prion diseases [4] [5] (including Creutzfeldt–Jakob disease and Gerstmann–Sträussler–Scheinker syndrome), [6] [7] [8] Alzheimer disease, [9] [10] and limbic and autoimmune encephalitis. [11] [12] He has served as the principal investigator on studies on human prion disease and Creutzfeldt-Jacob disease. [13] [1] He was guest editor for the American Academy of Neurology (AAN) Continuum Dementia edition, and was on the AAN committee for dementia criteria. [1] He has also published highly cited papers on cognitive dysfunction in movement disorders, [14] [15] and serves as the director of the MAC Huntington's Disease center. [16]

Biography

Like his brother Daniel Geschwind, Michael was inspired to study neurology by the work of Norman Geschwind, his father's cousin. [17] He majored in neurobiology in college, and obtained an M.D. and Ph.D. in neuroscience from Albert Einstein College of Medicine, [18] and went on to complete his internship at UCLA Medical Center, his residency at Johns Hopkins School of Medicine, and his fellowship at UCSF MAC. He currently holds the Michael J. Homer Chair in Neurology at UCSF MAC. [19]

He serves on the board of directors of the San Francisco Bay Area chapter of Physicians for Social Responsibility. [19]

Related Research Articles

<span class="mw-page-title-main">Creutzfeldt–Jakob disease</span> Degenerative neurological disorder

Creutzfeldt–Jakob disease (CJD), also known as subacute spongiform encephalopathy or neurocognitive disorder due to prion disease, is a fatal degenerative brain disorder. Early symptoms include memory problems, behavioral changes, poor coordination, and visual disturbances. Later symptoms include dementia, involuntary movements, blindness, weakness, and coma. About 70% of people die within a year of diagnosis. The name Creutzfeldt–Jakob disease was introduced by Walther Spielmeyer in 1922, after the German neurologists Hans Gerhard Creutzfeldt and Alfons Maria Jakob.

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

Parkinsonism is a clinical syndrome characterized by tremor, bradykinesia, rigidity, and postural instability. These are the four motor symptoms found in Parkinson's disease (PD) – after which it is named – dementia with Lewy bodies (DLB), Parkinson's disease dementia (PDD), and many other conditions. This set of symptoms occurs in a wide range of conditions and may have many causes, including neurodegenerative conditions, drugs, toxins, metabolic diseases, and neurological conditions other than PD.

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">Frontotemporal dementia</span> Types of dementia involving the frontal or temporal lobes

Frontotemporal dementia (FTD), or frontotemporal degeneration disease, or frontotemporal neurocognitive disorder, encompasses several types of dementia involving the progressive degeneration of frontal and temporal lobes. FTDs broadly present as behavioral or language disorders with gradual onsets. Common signs and symptoms include significant changes in social and personal behavior, apathy, blunting of emotions, and deficits in both expressive and receptive language. Currently, there is no cure for FTD, but there are treatments that help alleviate symptoms.

<span class="mw-page-title-main">Gerstmann–Sträussler–Scheinker syndrome</span> Human neurodegenerative disease

Gerstmann–Sträussler–Scheinker syndrome (GSS) is an extremely rare, always fatal neurodegenerative disease that affects patients from 20 to 60 years in age. It is exclusively heritable, and is found in only a few families all over the world. It is, however, classified with the transmissible spongiform encephalopathies (TSE) due to the causative role played by PRNP, the human prion protein. GSS was first reported by the Austrian physicians Josef Gerstmann, Ernst Sträussler and Ilya Scheinker in 1936.

<span class="mw-page-title-main">Primary progressive aphasia</span> Medical condition

Primary progressive aphasia (PPA) is a type of neurological syndrome in which language capabilities slowly and progressively become impaired. As with other types of aphasia, the symptoms that accompany PPA depend on what parts of the left hemisphere are significantly damaged. However, unlike most other aphasias, PPA results from continuous deterioration in brain tissue, which leads to early symptoms being far less detrimental than later symptoms.

Psychoorganic syndrome (POS), also known as organic psychosyndrome, is a progressive disease comparable to presenile dementia. It consists of psychopathological complex of symptoms that are caused by organic brain disorders that involve a reduction in memory and intellect. Psychoorganic syndrome is often accompanied by asthenia.

<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, tauopathies, 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">Limbic encephalitis</span> Inflammation involving the limbic system in the brain

Limbic encephalitis is a form of encephalitis, a disease characterized by inflammation of the brain. Limbic encephalitis is caused by autoimmunity: an abnormal state where the body produces antibodies against itself. Some cases are associated with cancer and some are not. Although the disease is known as "limbic" encephalitis, it is seldom limited to the limbic system and post-mortem studies usually show involvement of other parts of the brain. The disease was first described by Brierley and others in 1960 as a series of three cases. The link to cancer was first noted in 1968 and confirmed by later investigators.

<span class="mw-page-title-main">Variant Creutzfeldt–Jakob disease</span> Degenerative brain disease caused by prions

Variant Creutzfeldt–Jakob disease (vCJD), commonly referred to as "mad cow disease" or "human mad cow disease" to distinguish it from its BSE counterpart, is a fatal type of brain disease within the transmissible spongiform encephalopathy family. Initial symptoms include psychiatric problems, behavioral changes, and painful sensations. In the later stages of the illness, patients may exhibit poor coordination, dementia and involuntary movements. The length of time between exposure and the development of symptoms is unclear, but is believed to be years to decades. Average life expectancy following the onset of symptoms is 13 months.

<span class="mw-page-title-main">Kuru (disease)</span> Rare neurodegenerative disease caused by prions

Kuru is a rare, incurable, and fatal neurodegenerative disorder that was formerly common among the Fore people of Papua New Guinea. Kuru is a form of transmissible spongiform encephalopathy (TSE) caused by the transmission of abnormally folded proteins (prions), which leads to symptoms such as tremors and loss of coordination from neurodegeneration.

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.

<span class="mw-page-title-main">Variably protease-sensitive prionopathy</span> Medical condition

Variably protease-sensitive prionopathy (VPSPr) is a sporadic prion protein disease first described in an abstract for a conference on prions in 2006, and this study was published in a 2008 report on 11 cases. The study was conducted by Gambetti P., Zou W.Q., and coworkers from the United States National Prion Disease Pathology Surveillance Center. It was first identified as a distinct disease in 2010 by Zou W.Q. and coworkers from the United States National Prion Disease Pathology Surveillance Center.

<span class="mw-page-title-main">Autoimmune encephalitis</span> Type of encephalitis

Autoimmune encephalitis (AIE) is a type of encephalitis, and one of the most common causes of noninfectious encephalitis. It can be triggered by tumors, infections, or it may be cryptogenic. The neurological manifestations can be either acute or subacute and usually develop within six weeks. The clinical manifestations include behavioral and psychiatric symptoms, autonomic disturbances, movement disorders, and seizures.

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.

<span class="mw-page-title-main">Limbic-predominant age-related TDP-43 encephalopathy</span> (LATE) -- a form of dementia

LATE is a term that describes a prevalent condition with impaired memory and thinking in advanced age, often culminating in the dementia clinical syndrome. In other words, the symptoms of LATE are similar to those of Alzheimer's disease. 

Real-time quaking-induced conversion (RT-QuIC) is a highly sensitive assay for prion detection.

<span class="mw-page-title-main">Gladys Maestre</span> Venezuela-born Neuroscientist

Gladys Elena Maestre is a neuroscientist from Venezuela who is a professor at the University of Texas Rio Grande Valley School of Medicine. She is known for her work on Alzheimer's disease and other forms of dementia.

The Creutzfeldt-Jakob Disease Surveillance System (CJDSS) is a unit of the Public Health Agency of Canada. It studies the various variants of Creutzfeldt-Jakob Disease, and at least as of 2017, assisted "with DNA sequencing, autopsy and case confirmation". As of 2014, the CJDSS conducted "prospective national surveillance for all types of human prion disease in Canada. The main purposes of the CJDSS [were then] to better understand the epidemiology of human prion diseases, to improve the options available for their rapid and accurate diagnosis, and ultimately to protect the health of Canadians by reducing risks of prion disease transmission."

<span class="mw-page-title-main">Ava Easton</span>

Ava Easton is a health scientist and researcher who specialises in encephalitis, acquired brain injury and narrative medicine, and is considered a world expert in her field of Encephalitis patient outcomes and quality of life. She is the current Chief Executive of The Encephalitis Society, a non-profit organisation which provides support and resources for those affected by the neurological disease of Encephalitis, and collaborates with various organisations on research into the disease.

References

  1. 1 2 3 "Michael Geschwind | UCSF Profiles". profiles.ucsf.edu. Retrieved 2018-10-04.
  2. ↑ Geschwind, Michael D.; Shu, Huidy; Haman, Aissa; Sejvar, James J.; Miller, Bruce L. (July 2008). "Rapidly progressive dementia". Annals of Neurology. 64 (1): 97–108. doi:10.1002/ana.21430. ISSN   0364-5134. PMC   2647859 . PMID   18668637.
  3. ↑ Vitali, P.; Maccagnano, E.; Caverzasi, E.; Henry, R. G.; Haman, A.; Torres-Chae, C.; Johnson, D. Y.; Miller, B. L.; Geschwind, M. D. (2011-04-06). "Diffusion-weighted MRI hyperintensity patterns differentiate CJD from other rapid dementias". Neurology. 76 (20): 1711–9. doi:10.1212/WNL.0b013e31821a4439. ISSN   0028-3878. PMC   3100134 . PMID   21471469.
  4. ↑ Safar, Jiri G.; Geschwind, Michael D.; Deering, Camille; Didorenko, Svetlana; Sattavat, Mamta; Sanchez, Henry; Serban, Ana; Vey, Martin; Baron, Henry (2005-03-01). "Diagnosis of human prion disease". Proceedings of the National Academy of Sciences. 102 (9): 3501–3506. Bibcode:2005PNAS..102.3501S. doi: 10.1073/pnas.0409651102 . ISSN   0027-8424. PMC   552933 . PMID   15741275.
  5. ↑ Zou, Wen-Quan; Puoti, Gianfranco; Xiao, Xiangzhu; Yuan, Jue; Qing, Liuting; Cali, Ignazio; Shimoji, Miyuki; Langeveld, Jan P.M.; Castellani, Rudy (2010-08-02). "Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein". Annals of Neurology. 68 (2): 162–172. doi:10.1002/ana.22094. ISSN   0364-5134. PMC   3032610 . PMID   20695009.
  6. ↑ Young, Geoffrey S.; Geschwind, Michael D.; Fischbein, Nancy J.; Martindale, Jennifer L.; Henry, Roland G.; Liu, Songling; Lu, Ying; Wong, Stephen; Liu, Hong (2005-06-01). "Diffusion-Weighted and Fluid-Attenuated Inversion Recovery Imaging in Creutzfeldt-Jakob Disease: High Sensitivity and Specificity for Diagnosis". American Journal of Neuroradiology. 26 (6): 1551–1562. ISSN   0195-6108. PMC   8149066 . PMID   15956529.
  7. ↑ Geschwind, Michael D.; Martindale, Jennifer; Miller, Deborah; DeArmond, Stephen J.; Uyehara-Lock, Jane; Gaskin, David; Kramer, Joel H.; Barbaro, Nicholas M.; Miller, Bruce L. (2003-06-01). "Challenging the Clinical Utility of the 14-3-3 Protein for the Diagnosis of Sporadic Creutzfeldt-Jakob Disease". Archives of Neurology. 60 (6): 813–6. doi:10.1001/archneur.60.6.813. ISSN   0003-9942. PMID   12810484.
  8. ↑ Kolata, Gina Bari, 1948- (21 March 2017). Mercies in disguise : a story of hope, a family's genetic destiny, and the science that rescued them (First ed.). New York. ISBN   9781250064349. OCLC   966082972.{{cite book}}: CS1 maint: location missing publisher (link) CS1 maint: multiple names: authors list (link) CS1 maint: numeric names: authors list (link)
  9. ↑ Vossel, Keith A.; Beagle, Alexander J.; Rabinovici, Gil D.; Shu, Huidy; Lee, Suzee E.; Naasan, Georges; Hegde, Manu; Cornes, Susannah B.; Henry, Maya L. (2013-09-01). "Seizures and Epileptiform Activity in the Early Stages of Alzheimer Disease". JAMA Neurology. 70 (9): 1158–66. doi:10.1001/jamaneurol.2013.136. ISSN   2168-6149. PMC   4013391 . PMID   23835471.
  10. ↑ Coppola, Giovanni; Chinnathambi, Subashchandrabose; Lee, Jason JiYong; Dombroski, Beth A.; Baker, Matt C.; Soto-Ortolaza, Alexandra I.; Lee, Suzee E.; Klein, Eric; Huang, Alden Y. (2012-05-03). "Evidence for a role of the rare p.A152T variant in MAPT in increasing the risk for FTD-spectrum and Alzheimer's diseases". Human Molecular Genetics. 21 (15): 3500–3512. doi:10.1093/hmg/dds161. ISSN   0964-6906. PMC   3392107 . PMID   22556362.
  11. ↑ Lai, Meizan; Hughes, Ethan G.; Peng, Xiaoyu; Zhou, Lei; Gleichman, Amy J.; Shu, Huidy; Matà, Sabrina; Kremens, Daniel; Vitaliani, Roberta (April 2009). "AMPA receptor antibodies in limbic encephalitis alter synaptic receptor location". Annals of Neurology. 65 (4): 424–434. doi:10.1002/ana.21589. ISSN   0364-5134. PMC   2677127 . PMID   19338055.
  12. ↑ Graus, Francesc; Titulaer, Maarten J.; Balu, Ramani; Benseler, Susanne; Bien, Christian G.; Cellucci, Tania; Cortese, Irene; Dale, Russell C.; Gelfand, Jeffrey M.; Geschwind, Michael; Glaser, Carol A.; Honnorat, Jerome; Höftberger, Romana; Iizuka, Takahiro; Irani, Sarosh R.; Lancaster, Eric; Leypoldt, Frank; Prüss, Harald; Rae-Grant, Alexander; Reindl, Markus; Rosenfeld, Myrna R.; Rostásy, Kevin; Saiz, Albert; Venkatesan, Arun; Vincent, Angela; Wandinger, Klaus-Peter; Waters, Patrick; Dalmau, Josep (2016-04-01). "A clinical approach to diagnosis of autoimmune encephalitis". The Lancet Neurology. 15 (4): 391–404. doi:10.1016/S1474-4422(15)00401-9. ISSN   1474-4422. PMC   5066574 . PMID   26906964.
  13. ↑ Nedelman, Michael. "A 'family curse': First insomnia, then death". CNN. Retrieved 2018-10-04.
  14. ↑ Boxer, Adam L.; Geschwind, Michael D.; Belfor, Nataliya; Gorno-Tempini, Maria Luisa; Schauer, Guido F.; Miller, Bruce L.; Weiner, Michael W.; Rosen, Howard J. (2006-01-01). "Patterns of Brain Atrophy That Differentiate Corticobasal Degeneration Syndrome From Progressive Supranuclear Palsy". Archives of Neurology. 63 (1): 81–6. doi:10.1001/archneur.63.1.81. ISSN   0003-9942. PMID   16401739.
  15. ↑ Lee, J.- M.; Ramos, E. M.; Lee, J.- H.; Gillis, T.; Mysore, J. S.; Hayden, M. R.; Warby, S. C.; Morrison, P.; Nance, M. (2012-02-08). "CAG repeat expansion in Huntington disease determines age at onset in a fully dominant fashion". Neurology. 78 (10): 690–695. doi:10.1212/WNL.0b013e318249f683. ISSN   0028-3878. PMC   3306163 . PMID   22323755.
  16. ↑ "Michael Geschwind, MD, PhD". Memory and Aging Center. Retrieved 2018-10-04.
  17. ↑ Geschwind, Michael D. (29 May 2010). "Are you Related to "the Geschwind?"". Neuropsychology Review. 20 (2): 123–125. doi:10.1007/s11065-010-9135-9. ISSN   1040-7308. PMC   2881317 . PMID   20512417.
  18. ↑ "Health Professionals in Action: Dr. Michael Geschwind | SF Bay PSR". sfbaypsr.org. Retrieved 2018-10-04.
  19. 1 2 "Board of Directors | SF Bay PSR". sfbaypsr.org. Retrieved 2018-10-04.
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