Michael Mullan Alzheimers Research


The Roskamp Institute is devoted to understanding causes of and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. Based in Sarasota, Florida, the Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease.

Headed by Dr. Michael Mullan, the institute employs experienced and interdisciplinary scientists and technicians and houses state-of-the-art research labs and equipment to conduct scientific research. The quality of research performed at the institute reflects its motto: “Better science. Real discovery.”


Michael Mullan is a biomedical researcher of the β-amyloid protein and its relation to Alzheimer’s disease. Mullan’s Alzheimer research is well known among Biomedical Community. Dr. Mullan Alzheimer research work resulted in identifying the most widely known Swiss Mutation that is present in familial form. Transgenic Animal for Alzheimer Disease uses Swiss Mutation.

Dr. Mullan is currently the director[1] of the Roskamp Institute in Sarasota, Florida. Under Dr. Mullan’s guidelines the institute is carrying out cutting edge research in Alzheimer’s, Traumatic Brain Research, Gulf War Illness and other neuropsychiatric disorder.


Please visit websites to learn about Dr. Mullan Alzheimer’s Research Website:



Recent Posts

Antibodies Effectively Treat Alzheimer’s-like Disease

Drs. David Holtzman and Mac Diamond of the Washington University School of Medicine recently published research in Neuron that outlined the process of studying mice for potential tau protein tangle treatment avenues.

Tau is a toxic component of Alzheimer’s and other neurodegenerative diseases, due to the protein’s tendency to amass in tangles.  The aggregates, called neurofibrillary tangles, are believed to interfere with brain function and ultimately lead cognitive decline.  The study followed mice models with a neurodegenerative disease called frontotemporal dementia, whose tau proteins have similar pathology to those present in the brains of Alzheimer’s patients.  The scientists used advanced screening methods to sort through anti-bodies and identify the few that could stop uptake of accumulated tau by cellular interaction, therefore ending intracellular tau tangles.  The researchers then infused three anti-tau antibodies into mice brains.  The results showed mice with the anti-tau antibodies had reduced tau accumulation and increased cognition, while mice infused with control antibodies experienced no change.

The first study to deal with infusing antibodies directly into the brain, Washington University’s research not only suggests a path of action, but solidifies the spread of tau aggregates between cells as a crucial step in tau-mediated diseases like Alzheimer’s.  Dr. Diamond says that their research could lead to the creation of therapies designed to target the aggregation of tau proteins.


1) Kiran Yanamandra, Najla Kfoury, Hong Jiang, Thomas E. Mahan, Shengmei Ma, Susan E. Maloney, David F. Wozniak, Marc I. Diamond, David M. Holtzman.  Anti-tau Antibodies Block Tau Aggregates.  September 26, 2013. 10.1016/j.neuron.2013.07.046.

2) Washington University (September 26, 2013). Antibodies Effectively Treat Alzheimer’s-like Disease in Mice. Retrieved October  1, 2013 from http://www.sciencedaily.com/releases/2013/09/130926123326.htm

By Emma Henson

The Roskamp Institute is a 501(c)3 research facility dedicated to translating the efforts of its qualified research staff into real-world results for those suffering from neurological diseases. To learn more about our programs and to get information about donating, visit www.rfdn.org.

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  15. Dr. Michael Mullan Article Published in Herald Tribune: Dr. Michael Mullan: Volunteer to help fight Alzheimer’s Comments Off
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  17. Anti-Tumoral Activity of a Short Decapeptide Fragment of the Alzheimer’s Abeta Peptide. Comments Off
  18. Impaired orthotopic glioma growth and vascularization in transgenic mouse models of Alzheimer’s disease. Comments Off
  19. Characterization and use of human brain microvascular endothelial cells to examine β-amyloid exchange in the blood-brain barrier. Bachmeier C, Mullan M, Paris D. Comments Off
  20. Depletion of CXCR2 inhibits γ-secretase activity and amyloid-β production in a murine model of Alzheimer’s disease. Comments Off
  21. Selective antihypertensive dihydropyridines lower Aβ accumulation by targeting both the production and the clearance of Aβ across the blood-brain barrier. Comments Off
  22. Induction of drug efflux protein expression by venlafaxine but not desvenlafaxine. Comments Off
  23. Selective dihydropyiridine compounds facilitate the clearance of β-amyloid across the blood-brain barrier. Comments Off
  24. Feasibility of Predicting MCI/AD Using Neuropsychological Tests and Serum β-Amyloid. Comments Off
  25. Flavonoids lower Alzheimer’s Aβ production via an NFκB dependent mechanism. Comments Off
  26. Roskamp Institute in Sarasota, Florida, have shown that an anatabine compound supplied by Rock Creek has beneficial effects on memory and learning in animal models of Alzheimer’s Disease. Michael Mullan, MD, Ph.D., CEO of the Roskamp Institute and his colleague, Dr. Daniel Paris, published these findings in October, 2011 in the European Journal of Pharmacology Comments Off
  27. Mike Mullan Alzheimer Researcher Comments on: Nicotine May Help Combat Memory Loss study by Dr. Newhouse Comments Off
  28. Identification of Plasma Biomarkers of TBI Outcome Using Proteomic Approaches in an APOE Mouse Model. Comments Off
  29. Anatabine lowers Alzheimer’s Aβ production in vitro and in vivo Comments Off
  30. Elevated CSF levels of TACE activity and soluble TNF receptors in subjects with mild cognitive impairment and patients with Alzheimer’s disease. Comments Off
  31. Genetic deletion of TNF receptor suppresses excitatory synaptic transmission via reducing AMPA receptor synaptic localization in cortical neurons. Comments Off
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  41. Dr. Mullan’s Alzheimer Research Offers Invaluable Insights On The Disease Comments Off
  42. Dr. Mullan’s Alzheimer Research Identified Various Genetic Variations Comments Off
  43. Family History of Alzheimer’s disease – what does it mean? Comments Off
  44. ß-amyloid exchage in the blood-brain barrier Comments Off
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  46. Alzheimer’s disease drug developed at Roskamp Institute approved for key clinical trial funding in Europe Comments Off
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  48. Research Highlights The Direct Causes Related To The Disease Comments Off
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  50. Roskamp Institute researchers show that some antibodies but, not others may be helpful in removing the Alzheimer amyloid from the brain of Alzheimer’s sufferers. Comments Off
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  52. The Roskamp Institute investigates the role of anatabine in lowering Alzheimer’s Abeta levels. Comments Off
  53. Alzheimer Research Institute Headed By Dr. Michael Mullan Featured in the Sarasota Herald Tribune : Roskamp Institute research could help veterans Comments Off
  54. Dr. Mullan Alzheimer Presentation at Pines of Sarasota Comments Off
  55. Roskamp Institute Celebrated Veterans Day with a seminar by Alzheimer Researcher Dr. Michael Mullan Comments Off
  56. Alzheimer Expert Dr. Mullan’s comments on CD40L induces Abeta production via signaling by the granulocyte macrophage colony stimulating factor (GM-CSF) Comments Off
  57. Alzheimer Researcher Dr. Michael Mullans Note on Potent anti-angiogenic motifs within the Alzheimer beta-amyloid peptide. Comments Off
  58. Effect of NSAIDS on cognitive ability of Alzheimer’s Patient — Comment by Alzheimer Researcher Mullan Comments Off
  59. Dr. Mullan’s Alzheimer Research Notes on NSAIDS and their effect on Alzheimers disease Comments Off
  60. Roskamp Institute Gulf War Illness research program Comments Off
  61. Event: Journal Club “Disrupted-in-Schizophrenia-1 expression is regulated by β-site amyloid precursor protein cleaving enzyme-1–neuregulin cascade” Comments Off
  62. Event: Journal Club “The effect of encapsulated VEGF-secreting cells on brain amyloid load and behavioral impairment in a mouse model of Alzheimer’s disease” Comments Off
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  80. Anti-Tumoral Activity of a Short Decapeptide Fragment of the Alzheimer’s Abeta Peptide Comments Off
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  82. CD40/CD40L interaction induces Abeta production and increases gamma-secretase activity independently of tumor necrosis factor receptor associated factor (TRAF) signaling. Comments Off
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  93. Characteristics of thein VitroVasoactivity of β-Amyloid Peptides Comments Off
  94. Reduction of β-amyloid pathology by celastrol in a transgenic mouse model of Alzheimer’s disease Comments Off
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  121. Potent antiangiogenic motif in amyloid beta Comments Off
  122. CD40L induces Abeta production via signaling by the granulocyte macrophage colony stimulating factor (GM-CSF) Comments Off
  123. Potent anti-angiogenic motifs within the Alzheimer beta-amyloid peptide Comments Off
  124. Effect of NSAIDS on cognitive ability of Alzheimer’s Patients Comments Off
  125. NSAIDS and their effect on Alzheimers disease Comments Off
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