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| First Name: | John | | Last Name: | Ringman | | Title: | Associate Clinical Professor, Interim Director | | Advanced Degrees: | M.D., M.S. | | Affiliation: | Easton Center for Alzheimer's Disease Research | | Department: | UCLA Department of Neurology | | Street Address 1: | 10911 Weyburn Ave, #200 | | City: | Los Angeles | | State/Province: | CA | | Zip/Postal Code: | 90095-7226 | Country/Territory: | U.S.A. | | Phone: | (310) 794-3231 | | Fax: | (310) 794-3148 | | Email Address: |  |
Disclosure:
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Member reports no financial or other potential conflicts of interest. [Last Modified: 20 February 2011]
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View all comments by John Ringman
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Alzheimer Disease, Aging Process
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Brain imaging, Diagnosis, A-beta PP/A-beta, Clinical trials, Genetics
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Medical hospital, Research institute, University
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Dr. Ringman has a long-term interest in behavioral neurology, beginning as a student at the University of California at Berkeley where he received a Bachelor or Arts degree in Psychology and Neurobiology. He subsequently went to medical school at McGill University in Montreal, Canada and then completed a Neurology residency at Baylor College of Medicine in Houston, Texas. He received specialty training in behavioral neurology and dementia while a fellow working with Jeffrey Cummings and Mario Mendez at UCLA. Dr. Ringman then joined the Neurology faculty at the University of California at Irvine where he worked with Claudia Kawas and focused his interests on early diagnosis and treatment of Alzheimer's Disease. He returned to UCLA in 2003 and currently directs the UCLA Kagan Alzheimer's Disease Treatment Development Program and is performing studies characterizing the pre-clinical phase of familial Alzheimer's disease. He has a comprehensive research program in which persons with or at-risk for familial Alzheimer's disease due to known genetic alterations undergo cognitive, psychiatric, neuroimaging, and biochemical assessments. |
1) Increased fMRI signal with age in familial Alzheimer's disease mutation carriers. Braskie MN, Medina LD, Rodriguez-Agudelo Y, Geschwind DH, Macias-Islas MA, Cummings JL, Bookheimer SY, Ringman JM. Neurobiol Aging. 2010 Dec 1. PMID: 21129823
2) Effects of Risk Genes on BOLD Activation in Presymptomatic Carriers of Familial Alzheimer's Disease Mutations during a Novelty Encoding Task. Ringman JM, Medina LD, Braskie M, Rodriguez-Agudelo Y, Geschwind DH, Macias-Islas MA, Cummings JL, Bookheimer S.Cereb Cortex. 2010 Aug 20. PMID: 20729396
3) Distinct cerebrospinal fluid amyloid beta peptide signatures in sporadic and PSEN1 A431E-associated familial Alzheimer's disease. Portelius E, Andreasson U, Ringman JM, Buerger K, Daborg J, Buchhave P, Hansson O, Harmsen A, Gustavsson MK, Hanse E, Galasko D, Hampel H, Blennow K, Zetterberg H.
Mol Neurodegener. 2010 Jan 14;5:2. PMID: 20145736
4) Cortical event-related potentials in preclinical familial Alzheimer disease. Golob EJ, Ringman JM, Irimajiri R, Bright S, Schaffer B, Medina LD, Starr A.Neurology. 2009 Nov 17;73(20):1649-55. PMID: 19917987
5) Current concepts of mild cognitive impairment and their applicability to persons at-risk for familial Alzheimer's disease.
Ringman JM, Medina LD, Rodriguez-Agudelo Y, Chavez M, Lu P, Cummings JL. Curr Alzheimer Res. 2009 Aug;6(4):341-6.
PMID: 19689233
6) Commentary on "a roadmap for the prevention of dementia II: Leon Thal Symposium 2008." Prevention trials in persons at risk for dominantly inherited Alzheimer's disease: opportunities and challenges. Ringman JM, Grill J, Rodriguez-Agudelo Y, Chavez M, Xiong C. Alzheimers Dement. 2009 Mar;5(2):166-71. PMID: 19328453
7) Biochemical markers in persons with preclinical familial Alzheimer disease. Ringman JM, Younkin SG, Pratico D, Seltzer W, Cole GM, Geschwind DH, Rodriguez-Agudelo Y, Schaffer B, Fein J, Sokolow S, Rosario ER, Gylys KH, Varpetian A, Medina LD, Cummings JL.Neurology. 2008 Jul 8;71(2):85-92. Epub 2008 May 28. PMID: 18509095
8) Ringman JM, O'Neill J, Geschwind D, Medina L, Apostolova LG, Rodriguez Y, Schaffer B, Varpetian A, Tseng B, Ortiz F, Fitten J, Cummings JL, Bartzokis G. Diffusion Tensor Imaging in Preclinical and Presymptomatic Carriers of Familial Alzheimer's Disease Mutations. Brain. 2007 May 23. PMID: 17522104
9) Murrell J, Ghetti B, Cochran E, Macias-Islas MA, Medina L, Varpetian A, Cummings JL, Mendez MF, Kawas C, Chui H, Ringman JM. The A431E Mutation in PSEN1 causing Familial Alzheimer’s Disease Originating in Jalisco State, Mexico: An Additional Fifteen Families. Neurogenetics, 2006 Nov; 7(4):277-9. PMID: 16897084
10) Ringman JM, Diaz-Olavarrietta C, Rodriquez Y, Chavez M, Fairbanks L, Paz F, Varpetian A, Maldonado HC, Macias-Islas MA, Murrell J, Ghetti B, Kawas C. Neuropsychological function in nondemented carriers of presenilin-1 mutations. Neurology, 2005; Aug 23;65(4):552-558. PMID: 16116115 |
Regarding Alzheimer's disease (AD), I feel the greatest void in our knowledge is our lack of understanding the connection between overproduction and/or decreased degradation of Abeta42 and the neurofibrillary pathology and neuronal death that are the most direct cause of patients' symptoms and signs. |
1) Decreased clearance of CNS beta-amyloid in Alzheimer's disease. Mawuenyega KG, Sigurdson W, Ovod V, Munsell L, Kasten T, Morris JC, Yarasheski KE, Bateman RJ.
Science. 2010 Dec 24;330(6012):1774. Epub 2010 Dec 9. PMID: 21148344
2) Pre-dementia clinical stages in presenilin 1 E280A familial early-onset Alzheimer's disease: a retrospective cohort study.
Acosta-Baena N, Sepulveda-Falla D, Lopera-Gómez CM, Jaramillo-Elorza MC, Moreno S, Aguirre-Acevedo DC, Saldarriaga A, Lopera F. Lancet Neurol. 2011 Feb 3. PMID: 2129602
3) Hippocampal hyperactivation in presymptomatic familial Alzheimer's disease. Quiroz YT, Budson AE, Celone K, Ruiz A, Newmark R, Castrillón G, Lopera F, Stern CE.
Ann Neurol. 2010 Dec;68(6):865-75. PMID: 21194156 |
I would focus my efforts on performing drug trials in persons with or at-risk for familial AD as this is a population in whom prevention of the disease could be reliably demonstrated. |
I think that Alzheimer's disease is actually a group of illnesses with a similar phenotype. That is, there are different ways of arriving at the common pathway of dementia associated with amyloid plaques and neurofibrillary tangles. I am biased towards genetic causes and believe that each case of late-onset AD can ultimately be attributed to contributions from multiple, some as yet unidentified, genes. The connections between genetic variations and the disease are very complicated and will be hard to disentangle. For instance, even in Presenilin-1 associated AD, our knowledge of the normal functions of PS1 is still evolving. |
A comprehensive understanding of the human genome and the ways the protein products of these genes interact to create all of human physiology. I am aware this is a tall order. |
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