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Rakez Kayed, Ph.D
Assistant
Professor
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Director:
The Kayed Laboratory
Publications via PubMed
http://www.ncbi.nlm.nih.gov/pubmed?term=kayed%20R
PUBLICATIONS: 2007-2011
1.
C. A.
Lasagna-Reeves, D. Castillo-Carranza, U. Sengupta, J. Sarmiento,
J. Troncoso, G. R. Jackson, and R. Kayed; “Alzheimer
Brain-Derived Tau Species Are Authentic Oligomers with Potent
Amnestic Effects in Vivo”.
Submitted.
2.
C. A.
Lasagna-Reeves, and R. Kayed; “Astrocytes
contain amyloid-β annular protofibrils in Alzheimer’s disease
brains”. Submitted.
3.
S. Rasool, H.
Martinez-Coria, L. Breydo, J. Wu, S. Milton, A. Tran, R. Albay,
R. Kayed, and C. Glabe ; “vaccination
with a non-human random sequence amyloid oligomer mimic results
in improved cognitive function and reduced plaque deposition in
Tg2576 mice". Submitted.
4.
A. L.
Clos, C. A. Lasagna-Reeves, D. Castillo-Carranza, U. Sengupta,
G. R. Jackson, B. Kelly, T. M. Beachkofsky and R. Kayed;
“Formation
of immunoglobulin light chain amyloid oligomers
in primary nodular cutaneous
amyloidosis”. British Journal of Dermatology.
Online 07/2011, PMID 21729025.
5.
C. A.
Lasagna-Reeves, D. Castillo-Carranza, U. Sengupta, A. L. Clos,
G. R. Jackson and R. Kayed; “Tau oligomers impair memory
and induce synaptic and mitochondrial dysfunction in wild type
mice”. Molecular Neurodegeneration.
2011 6; 6(1):39.
(Most
accessed research article in the first 30 days of its
publication).
6.
A. L. Clos, C. A.
Lasagna-Reeves, B. Kelly, R. Wagner, M. Wilkerson, G. R.
Jackson, R. Kayed; “Role of Oligomers in the
Amyloidogenesis of Primary Cutaneous Amyloidosis”.
(JAAD),
2011, PMID: 21669474DOI:10.1016/j.jaad.
7.
C. A.
Lasagna-Reeves, C. G. Glabe and R. Kayed;
“Amyloid-β annular protofibrils evade the fibrillar fate in
Alzheimer’s disease brains”. J Biol Chem.
2011, 286(25):22122-30. (Selected
as Paper of the week, top 1% of papers published in J Biol Chem.)
8.
R. Kayed,
G. R. Jackson, D. M. Estes, and A. D.T. Barrett; “Alzheimer’s
disease: Review of Emerging Treatment Role for Intravenous
Immunoglobulins. Journal of Central Nervous System Disease”.
2011: 3 67-73; DOI:
10.4137/JCNSD.S5018.
9.
R. Kayed;
“Tau oligomers as potential drug target for Alzheimer`s disease
treatment”. "Alzheimer's Disease / Book 2", ISBN
978-953-307-466-5. InTech Press, Vienna, 2010.
10.
C. A.
Lasagna-reeves, D. L. Castillo-Carranza, G. R. Jackson and R.
Kayed; “Tau oligomers as potential target for immunotherapy
for Alzheimer disease and tauopathies”. Current Alzheimer
Research. 05/2011, PMID: 21605039.
11.
L. Zepa, M. Frenkel,
H. Belinson, Z. Kariv, R. Kayed, E. Masliah, and D. M.
Michaelson; “ ApoE4-driven accumulation of intraneuronal
oligomerized Aβ42 following activation of the amyloid cascade in
vivo is mediated by a gain of function”. International
Journal of Alzheimer1s Disease (IJAD),
2011 (doi:10.4061/2011/792070).
12.
C. A.
Lasagna-reeves; D. L. Castillo-carranza,
M. J. Guerrero-Munoz, G. R.
Jackson, and R. Kayed; “Preparation and characterization
of neurotoxic tau oligomers”. Biochemistry;
2010; 49(47); 10039-10041. (Most read research article in
the first 30 days of its publication).
13.
R. Kayed
and C. A. Lasagna-reeves; “Amyloid hypothesis: Molecular and
cellular aspect of toxicity”. Alzheimer`s Disease; Editor,
Philippe Derreumaux, Imperial College Press, London, 2010.
14.
H. Belinson, Z.
Kariv, R. Kayed, E. Masliah, and D. M. Michaelson;
“Pathological synergism between oligomerized Aβ and
apolipoprotein E4”. Journal of Alzheimer`s Disease (JAD),
2010. 1, 22, (3),
959-70.
15.
R. Kayed,
I. Canto, L. Breydo, S. Rasool, J. Wu, R. Albay, A. Pensalfini,
and C. Glabe;
“Monoclonal Antibodies
Distinguish Different Strains of Prefibrillar Aß Oligomers”,
Molecular Neurodegeneration,
2010, 13; 5: 57.
(Most accessed research
article in the first 30 days of its publication)
16.
R. Kayed;
“Anti-tau oligomers vaccine
for the treatment of Alzheimer’s disease: Opportunities and
challenges”. Human Vaccines, 2010; 6; 47-51.
17.
C. A.
Lasagna-Reeves, A. L. Clos, M-H Terumi, R. M. Goldblum, G. R.
Jackson, and R. Kayed;
“Inhaled insulin forms toxic pulmonary amyloid aggregates”,
Endocrinology, 2010;151(10):4717-24.
18.
A. L. Clos, C. A.
Lasagna-Reeves, R. Wagner, B. Kelly, G. R. Jackson and R.
Kayed; “Therapeutic removal of amyloid deposits in cutaneous
amyloidosis by localized intralesional injections of anti-amyloid
antibodies”. Experimental
Dermatology. 2010; 19(10):904-11.
19.
K. T. Dineley, R. Kayed, V. Neugebauer, W. Zhang and G. Taglialatela;
“Amyloid beta oligomers impair fear conditioning memory
in a calcineurin-dependant fashion in mice”.
J Neurosci Res, 88(13): 2923-32, 2010.
20.
C. M. Hernandez, R. Kayed, H. Zheng, J. D. Sweat, and K. T. Dineley;
“Nicotinic receptors enhances Aβ oligomers accumulation
exacerbating early-stage cognitive decline and septo-hippocampal
pathology in a mouse model of Alzheimer`s disease”.
Journal of Neuroscience, 30: 2442 – 2453, 2010.
21.
A.
Barrett, R. Kayed, G. R. Jackson, K. Cunningham; “ New
vaccine development for chronic brain diseases”.
Neuropsyhopharmacology, 35, 1: 354, 2010.
22.
E. Head, V. Pop, F.
Sarsoza, R. Kayed, T. Beckett, C. M. Studzinski, J. L.
Tomic, C. G. Glabe, and M. P Murphy; “Amyloid
β-peptide oligomers in brain and CSF of aged canines”.
Journal of Alzheimer`s Disease, 20(2): 637-462,
2010.
23.
J. M. Isas, V.
Luibl, L. V. Johnson, R. Kayed, R. Wetzel, C. G. Glabe,
R. Langen, and J. Chen;” Soluble and mature amyloid
fibrils in Drusen deposits”. Invest. Ophthalmol. Vis.
Sci. , 51: 1304 – 1310, 2010.
24.
R. Kayed,
and G. R. Jackson;
“Pre-filament tau species as potential targets for immunotherapy
for Alzheimer disease and related disorders”. Current.
Opinions in Immunology. 21(3): 359-63, 2009.
25.
H.
Kokubo, R. Kayed, C. G. Glabe, T. C. Saido, and H.
Yamaguchia; “Amyloid beta annular protofibrils in cell processes
and synapses accumulate with aging and Alzheimer-associated
genetic modification” International Journal of Alzheimer's Disease (IJAD),
Volume 2009 , Article ID 689285, 7
pages
doi:10.4061/2009/689285, 2009.
26.
E. W. Mina, C.
Lasagna-Reeves, C. G. Glabe, and
R. Kayed “Poloxamer P188 copolymer membrane sealant rescues
membrane permeabilization and toxicity of amyloid oligomers in vitro” ;
Journal of Molecular Biology, 391,
3, 577–585, 2009.
27.
K.
Yanamandra, O. Alexeyev, V. Zamotin, V. Srivastava, T. Vogl, R. Kayed, G. Wingsle, J. Olsson, C. M. Dobson, A. Bergh, F.
Elgh, and L. A. Morozova-Roche; “Pro-inflammatory S100A8/A9
proteins in prostate amyloidosis and dystrophic calcification”.
Plos One,
4, 5, 2009.
28.
F. Sarsoza, R.
Kayed, R. Dahlin, M. Dick, C. Broadwater-Hollifield, S.
Mobley, I. Lott, E. Doran, D. Gillen, C. Anderson-Bergman, D. H.
Cribbs, C. Glabe, and E. Head; “
A fibril specific, conformation dependent antibody recognizes a
subset of Aβ plaques and angiopathy in Alzheimer disease, Down
syndrome and Tg2576 transgenic mouse brain”;
Acta Neuropathologica, 118, 4, 505–517,2009.
29.
R.
Kayed,
A. Pensalfini, L. Margol,
Y. Sokolov, F. Sarsoza, E. Head, James Hall,
and C. G. Glabe; “Annular protofibrils are a structurally and
functionally distinct type of amyloid oligomer” J. Biol.
Chem., 284: 4230 – 4237, 2009.
30.
L. C.
Reese, W. Zhang, K. T. Dineley, R. Kayed, and G.
Taglialatela; “Selective induction of calcineurin activity and
signaling by oligomeric amyloid beta”. Aging Cell,
7(6): 824-35, 2008.
31.
T. M.
Shin, J. M. Isas, R. Kayed, C. G. Glabe , R. Langen, and
J. Chen ; “Formation of soluble oligomeric and amyloid
species of the multifunctional protein vitronectin”
Molecular Neurodegeneration,
3: 16, 2008.
32.
M. Bacher, R. Dodel,
B. Aljabari, K. Keyvani, P. Marambaud, R. Kayed, C. G.
Glabe, N. Goertz, Hoppmann, N. sachser, J. Klotsche, L.
Lewejohann, and Y. Al-Abed; “CNI-1493 inhibits Aβ production,
plaque formation, and cognitive deterioration in an animal model
of Alzheimer’s disease”. J. Exp. Med., 205:1593-1599,
2008.
33.
R. Kayed,
E. Head, F. Sarsoza, T. Saing, M. Necula, L. Margol, J. Wu, L.
Breydo, J. L. Thompson, S. Rasool, T. Gurlo, P. C. Butler and
C. G. Glabe; “Fibril specific, conformation dependent antibodies
recognize a generic epitope common to amyloid fibrils and
fibrillar oligomers that is distinct from prefibrillar oligomers”
Molecular Neurodegeneration, 2:18,2007. (Highly
accessed research article)
34.
Y. Yoshiike, R.
Kayed, S. C Milton, A. Takashima, and C. G Glabe;
“Pore-Forming Proteins Share Structural and Functional Homology
with Amyloid Oligomers”. Neuromolecular Med., 9 (3):
270-275, 2007.
35.
M. Necula, R.
Kayed, S. Milton, and C. G. Glabe; “Small-molecule
inhibitors of aggregation indicate that amyloid beta
oligomerization and fibrillization pathways are independent and
distinct”. J. Biol. Chem., 282: 10311-10324, 2007.
36.
A. Maloyan, J.
Gulick, C. G. Glabe, R. Kayed, and J. Robbins; “Exercise
reverses preamyloid oligomer and prolongs survival in  B-crystallin-based
desmin-related cardiomyopathy”. PNAS, 104, 5995– 6000,
2007.
37.
M. Necula, L.
Breydo, S.Milton, R. Kayed, W. E. van der Veer, P. Tone,
and C. G.Glabe; “Methylene bluei nhibits amyloid Aβ
oligomerization by promoting fibrillization” Biochemistry,
46(30); 8850-8860, 2007.
38.
O. Wirths, J.
Weis, R. Kayed, T. C. Saido, and T .A. Bayer;
“Age-dependent axonal degeneration in an Alzheimer mouse model”.
Neurobiology of Aging, 28(11): 1689-99, 2007.
39.
C.-Y. Lin, T. Gurlo, R. Kayed, A. E. Butler, L. Haataja, C. G. Glabe, and P.
C. Butler, Toxic human islet amyloid polypeptide (h-IAPP)
oligomers are intracellular, and vaccination to induce
anti-toxic oligomer antibodies in h-IAPP transgenic mice, Diabetes, 56: 1324-1332, 2007.
40.
J. Zhou, M.I.
Fonseca, L. Billings-Luhr, R. Kayed, C.G. Glabe, F.
LaFerla, and A. J. Tanner, “Effect of immunization with the
oligomeric form of the Aβ peptide: Reduction of senile plaque
area, decreased complement C3 deposition and synthesis, and
decline in behavioral function in a murine model of Alzheimer's
disease”. Molecular Immunology, 44, 1-3, 264-265, 2007.
SELECTED PAPERS PUBLISHED BEFORE 2007
1.
R. Kayed,
and C. G. Glabe; “Conformation-dependent anti-amyloid oligomer
antibodies”. Methods in Enzymology, 413, 326-344, 2006.
2.
C. G. Glabe, and R. Kayed; “Common structure and toxic function of amyloid
oligomers implies a common mechanism of pathogenesis”. Neurology, 24; 66, 74-78, 2006.
3.
J.
Meier, R. Kayed, C.-Y Lin, T. Gurlo, L. Haataja, S.
Jayasinghe, R. Langen, C. G. Glabe, and P. C. Butler;
“Inhibition of hIAPP fibril formation does not prevent beta-cell
death: Evidence for distinct actions of oligomers and fibrils of
hIAPP”. Am. J. Physiol. Endocrinol. Metab. , 291,
1317-1324, 2006.
4.
V. Luibl, J. M.
Isas, R. Kayed, C. G. Glabe, R. Langen, and J. Chen;
“Drusen deposits associated with aging and age-related macular
degeneration contain non-fibrillar amyloid oligomers”. Journal of Clinical investigation, 116, 2, 378-385, 2006.
5.
S. Lesne, M. T. Koh,
L. Kotilinek, R. Kayed, C. G. Glabe, A. Yang, M.
Gallagher, and K. H. Ashe; “Aspecific amyloid-β protein assembly
in the brain impairs memory”. Nature, 440, 7082:352-7,
2006.
6.
J. Zhou, M. I.
Fonseca, R. Kayed, S. D. Webster, I. Hernandez, O. Yazan,
D. H. Cribbs, C. G. Glabe, and A. J. Tenner; “Novel A-beta
peptide immunogens modulate plaque pathology and inflammation in
a murine model of Alzheimer's Disease”. Journal of
Neuroinflammation, 2, 28 2-23, 2005.
7.
A. Sanbe, H.
Osinska, C. Villa, R. Klevitsky, C. G. Glabe, R. Kayed,
and J. Robbins; “Reversal of amyloid-induced heart disease in
desmin-related cardiomyopathy”. PNAS, 102, 13592 –13597,
2005.
8.
H. Kokubo, R.
Kayed, C. G. Glabe, T. C. Saido, N. Iwata, J. B. Helms, and
H. Yamaguchi; “Soluble Aβ oligomers ultrastructurally localize
to cell processes, especially to axon terminal with higher
density, but not to lipid rafts in Tg2576 mouse brain”. Brain
Research, 1045, 1-2, 224-228, 2005.
9.
Demuro, E. Mina, R. Kayed, I. Parker, and C. G. Glabe; “Calcium dysregulation
and membrane disruption as a ubiquitous mechanism of amyloid
oligomer-mediated neurotoxicity”. J. Biol. Chem., 280,
17, 17294-300, 2005.
10.
L. Asatryan, R. T.
Hamilton, J. M. Isas, J. Hwang, R. Kayed, and A. Sevanian;
“LDL phospholipid hydrolysis produces modified electronegative
particles with an unfolded apoB100 protein”. J. Lipid Res.,
46, 1,115-122, 2005.
11.
R. Kayed,
Y. Sokolov, B. Edmonds, T. M. McIntire, S. C. Milton, J. E.
Hall, and C. G. Glabe; “Permeabilization of lipid bilayers is a
common conformation-dependent activity of soluble amyloid
oligomers in protein misfolding diseases”. Accelerated
publication J. Biol. Chem., 279(45):46363-46366,
2004.
12.
H. Kokubo, R.
Kayed, C. G. Glabe, and H. Yamaguchi; “Soluble Aβ oligomers
ultrastructurally localize to cell processes and might relate
with synaptic dysfunction in Alzheimer’s disease brain”.
Brain Research, 1031, 2, 222-228, 2004.
13.
A. Sanbe, H.
Osinska , J. E. Saffitz, C. G. Glabe , R. Kayed , A.
Maloyan, and J. Robbins; “Desmin-related cardiomyopathy in
transgenic mice: A cardiac amyloidosis”. PNAS, 101, 27,
10132-10136, 2004.
14.
S. Oddo, A. Caccamo,
J. D. Shepherd, M. P. Murphy, T. E. Golde, R. Kayed, R.
Metherate, M. P. Mattson, Y. Akbari, and F. M. LaFerla; “Triple
transgenic model of Alzheimer’s disease with plaques and
tangles: Intracellular Aß and synaptic dysfunction”. Neuron,
31; 39, 3:409-21, 2003.
15.
R. Kayed,
E. Head, J. L. Thompson, T. M. McIntire, S. C. Milton, C. W.
Cotman, and C. G. Glabe; “Common structure of soluble amyloid
oligomers implies common mechanism of pathogenesis”. Science,
300, 486–489, 2003.
ABSTRACTS and PRESENTATIONS: 2009-2011
1.
R. Kayed;
“Tau oligomers as a biomarker for neurodegeneration au oligomer
in AD and neurodegenerative tauopathies”. 2nd
International conference on Neurodegenerative disorders:
immunotherapy and biomarkers, Uppsala, Sweden, 2011. Featured:
(Link)
2.
ASN, American
Society for Neurochemistry 2011 meeting, St. Louis, Missouri;
March 2011.
3.
R. Kayed;
“Tau oligomer in AD and neurodegenerative tauopathies”. ASN,
American Society for Neurochemistry 2011 meeting, St. Louis,
Missouri; March 2011.
4.
C. A.
Lasagna-Reeves, U. Sengupta, and R. Kayed; “Cellular
mechanism involved in tau oligomers neurotoxicity”. The SFN 40th
annual meeting, 11/2010, San Diego, CA
5.
C. A.
Lasagna-Reeves, M. J. Guerrero-Munoz, U. Sengupta, J. Troncoso,
G. R. Jackson, and R. Kayed; “Characterization of tau
oligomers in Alzheimer`s disease”. The SFN 40th
annual meeting, 11/2010, San Diego, CA. Featured at AlzForum:
(Link)
6.
D. L. Castillo-Caranza,
C. A. Lasagna-Reeves, M. J. Guerrero-Munoz, D. M. Estes, A.
Barrett, K. Dineley, G. R. Jackson, and R. Kayed;
“Modulation of tau oligomers by passive vaccination”. The SFN 40th
annual meeting, 11/2010, San Diego, CA. Featured in Neurology Today
(Link) and AlzForum
(Link)
7.
C. A.
Lasagna-Reeves, M. J. Guerrero-Munoz, D. L. Castillo-Caranza, U.
Sengupta, J. Troncoso, G. R. Jackson, and R. Kayed; “Tau
oligomers in Parkinson disease and Dementia with Lewy Bodies and
their connection with α-synuclein oligomers”. The SFN 40th
annual meeting, 11/2010, San Diego, CA.
8.
M. J.
Guerrero-Munoz, C. A. Lasagna-Reeves and R. Kayed;
“Characterization and relevance of novel anti-oligomer mouse
monoclonal antibody”. The SFN 40th annual meeting,
11/2010, San Diego, CA.
9.
C. A.
Lasagna-Reeves, B. Roi, M. J. Guerrero-Muñoz, D. L.
Castillo-Carranza, R. Kayed and G.R. Jackson; “Role of
Tau oligomers in Parkinson’s disease (PD) and Lewy body dementia
(DLB) ”. 14th International Congress of Parkinson’s
disease and Movement Disorders. Buenos Aires, Argentina, June
13-17, 2010. Was chosen for the highlight blue ribbon session.
10.
D. L.
Castillo-Carranza, C. A. Lasagna-Reeves, M.J. Guerrero-Muñoz, J.
Troncoso, G.R. Jackson and R. Kayed; “Alpha-synuclein
oligomers in Parkinson’s disease (PD) and Lewy body dementia (DLB)
”. 14th International Congress of Parkinson’s disease
and Movement Disorders. Buenos Aires, Argentina, June 13-17,
2010.
11.
C. A.
Lasagna-Reeves, J. Troncoso, G.R. Jackson and R. Kayed;
“The formation of pore-like amyloid aggregates in movement
disorders”. 14th International Congress of
Parkinson’s disease and Movement Disorders. Buenos Aires,
Argentina, June 13-17, 2010.
12.
A. L. Clos, C. A.
Lasagna-Reeves, R. Wagner, M. Pettit, G.R. Jackson, B. Kelly and
R. Kayed;“Aggregation of essential proteins in skin
cancer”. UTMB Comprehensive Cancer Center Day, Galveston, TX,
USA, May 18th 2010.
13.
A. L. Clos, C. A.
Lasagna-Reeves, R. Wagner, M. Pettit, G.R. Jackson, B. Kelly and
R. Kayed;“Therapeutic removal of amyloid deposits by anti
amyloid antibodies. 70th Society for Investigative
Dermatology annual meeting. Atlanta, Georgia, USA, May 5-8,
2010.
14.
M. J. Guerrero-Muñoz,
C. A. Lasagna-Reeves and R. Kayed; “Novel anti-oligomer
Mouse monoclonal antibodies; Characterization and relevance”. 13th
Annual Forum on Aging, UTMB, Nov. 2009.
15.
C. A.
Lasagna-Reeves, G.R. Jackson and R. Kayed; “Tau oligomers
in Alzheimer’s disease and others tauopathies”. 13th
Annual Forum on Aging, UTMB, Nov. 2009. (First place in
Neurosciences category, for graduate student).
16.
D. L.
Castillo-Carranza, C. A. Lasagna-Reeves, G.R. Jackson and R.
Kayed; “Induction of protein aggregation by preformed
amyloid oligomers”. 13th Annual Forum on Aging, UTMB,
Nov. 2009.
17.
A. L. Clos, C.
Lasagna-Reeves, G.R. Jackson, B. Kelly and R. Kayed;
“Therapeutic approaches to amyloidosis: implication for
neurodegenerative diseases”. 13th Annual Forum on
Aging, UTMB, Nov. 2009. (First place in Neurosciences category,
for MD students).
18.
Lasagna-Reeves, G.R.
Jackson and R. Kayed; “Tau oligomers in Alzheimer’s
disease”. The SFN 39th annual meeting, 10/2009,
Chicago, IL. Covered by Alzforum:
(Link)
19.
G. Taglialatela, L.
C. Reese, Z. Martin, W Zhang, K. T. Dineley, V. Neugebauer, and
R. Kayed;“Alpha synuclein oligomers induce calcineurin-dependent
neurobehavioral deficits”. The SFN 39th annual
meeting, 10/2009, Chicago, IL.
20.
R. Kayed,
C. A. Lasagna-Reeves and G.R. Jackson; “Tau annular protofibrils
in Neurodegerative diseases”. The SFN 39th annual
meeting, 10/2009, Chicago, IL.
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