RETIRED July 1, 2008

Education

Research Interests

1. Alzheimer's Disease and the role of b-amyloid fragments in the neurobiology of AD:

I am studying the potential mechanisms of neurotoxicity of the Beta Amyloid protein fragment (A beta 1-42) with attention directed at the signaling pathways activated by A beta 1-42 in rat neurons challenged with the fragment and dying consequently by apoptosis. My results indicate that A beta 1-42 is neurotoxic to neurons in the septum/diagonal band, cerebral cortex and the hippocampus and thus may play a role in the cell loss seen in Alzheimer's disease. The Ab fragments induced apoptosis in all areas tested.

The AB1-42 fragment may utilize the NMDA subtype of the glutamate receptor in the expression of its neurotoxicity. The NMDA receptors are present at high density in regions CA1 and CA3 of the hippocampus and in slightly lower numbers within the dentate gyrus. Co-injection of equimolar AB1-42 and AP-5 (NMDA receptor antagonist) attenuated the toxicity of AB1-42. The lesions were serially reconstructed and their calculated volumes revealed that the AB1-42 lesion volume was 5-7 times larger than the AB1-42/AP-5 induced lesion. AB1-42/AP-5 resulted in a limited localized reduction of the pyramidal cells in CA1, while AB1-42 alone destroyed pyramidal cells and many granule cells in the dentate gyrus. Co-injection of magnesium chloride (1.5 mM), a noncompetitive blocker of the Ca⁺2 channel of the NMDA receptor, had an effect similar to AB1-42/AP-5.

Extracellular challenge of hippocampal neurons with AB1-42 induces oxidative stress (free radical production), lipid peroxidation and disturbances of calcium homeostasis. It is clear that the AB1-42 fragment interacts with the plasma membrane; however, the signaling pathways leading to apoptosis or other avenues of cell death still need to be resolved. Pyramidal cells of the hippocampus show immunoreactivity for caspase 3 (a cysteine protease involved in apoptosis) following challenge with AB1-42. There is evidence that p53 and BAX must be activated prior to activation of caspase 3 which then migrates to the cell nucleus to disrupt PARP ( Poly-[ADP-Ribose] Polymerase) and as a consequence the cell fails to repair breaks in the DNA and the cell dies. Hippocampal pyramidal neurons after challenge with AB1-42, are immunoreactive for cytochrome c indicating that this mitochondrial protein has been lost by the mitochondria and spilled into the cytosol. Loss of cytochrome c from mitochondria suggests mitochondrial dysfunction and indicates the involvement of an additional signaling pathway leading to apoptosis.

The AB1-42 fragment is present within cells (both neurons and glia) and this intracellular peptide fragment may act within the cell to induce cell death. I am using electron microscopy immunogold in an effort to identify organelles with which AB may interact. In Alzheimer's disease there is an increase in intracellular AB1-42 and by treating neurons in rats with chloroquine (an alkaline, endosomal-lysosomal inhibitor) intracellular levels of AB are elevated. Neurons in the rat hippocampus were challenged in vivo with chloroquine (20-60 uM) and the brains fixed by intra-cardiac perfusion of 4% paraformaldehyde/0.5% glutaraldehyde (pH7.5). Tissue blocks from the hippocampus were processed and embedded in Lowicryl. The double-bridge technic of Sternburger was used to immunostain tissue sections. Thin sections (60 nm) were immunostained with a primary antibody specific to AB1-42 (midregion AA 17-24) and a secondary antibody conjugated to 40 nm gold. A second primary antibody specific for the C-terminal of AB1-42, was utilized and was coupled to a secondary antibody conjugated to a 15m gold particle. Gold particles 40 and 15 nm were found in the rough endoplasmic reticulum (RER), the nucleus and mitochondria which is indicative of double labeled AB1-42 associated with these membranes and organelles. Further, I have localized in the RER Presenilin 1 (PS1), the -secretase enzyme involved in the production of AB1-42. I used a new antibody specific to PS1, tagged it with a secondary antibody conjugated with Texas Red (Fluorochrome) and examined the tissue by confocal microscopy. The cytoplasm of the hippocampal pyramidal cell fluoresced red, indicating that the tagged PS1 was present. The PS1 antibody was used in an immunogold study and the PS1 was localized to the RER. Both PS1 and AB1-42 are localized in the RER suggesting that AB1-42 is cleaved from the APP precursor protein while in the RER compartment rather than the endosomal compartment. The early appearance of AB1-42 provides the opportunity for the fragment to migrate to other membrane compartments. That AB1-42 targets the RER, nucleus and mitochondria is significant in that these organelles provide sites of interaction between the membranes and AB1-42 leading to cell death, apoptosis and Alzheimer’s disease. I am exploring in more detail the possible interactions of the intracellular membranes and the AB1-42 fragment an understanding of which is important in the development of an effective therapy for control of Alzheimer’s disease.

I have demonstrated the presence of AB1-42 or polymers of AB1-42 (possible tetramers) in the endoplasmic reticulum isolated from tissues (frontal lobe and temporal lobe) of patients with Alzheimer’s Disease. Tissues were obtained from the Alzheimer Disease Research Center- Brain Bank, University of Washington, Seattle, WN. Intracellular AB-peptides may exist as tetramers in the membranes of the endoplasmic reticulum (ER) and mitochondria (M) in rat and human brain. A 17.6 kDa (AB-tetramer) was identified in Western Blot of rat ER & M, while in human brain ER (AD & controls) an 18 kDa AB-tetramer was detected. We argue that the AB-tetramers are present in membranes of organelles critical to normal cellular functions, and may alter biological functions leading to cell death and AD. The significance of these observations remains to be determined.

2. Microvasculature of the rat brain as a model for the pathophysiology of stroke.

My work with the rat cerebral vascular system involves vascular endocasts, scanning electron microscopy, and histochemistry of various enzymes in the walls of aging arteries supplying the cerebral cortex, striatum, thalamus and midbrain. The vascular studies are designed to define arterial patterns in specific parts of the rat brain, and compare these patterns to the patterns in analogous parts of the human brain. The rat cerebral vasculature studied to date closely resembles the patterns seen in human brain, consequently the rat may be used to evaluate changes in the metabolic profiles of stroke prone vessels in relation to aging and to experimentally induced hypertension.

Institutional Faculties

1. Medical School Faculty, Hahnemann University, 1973–1978
2. Graduate School Faculty, Hahnemann University, 1974–1978
3. School of Allied Health, Hahnemann University, 1973–1978
4. Medical College Faculty, Texas A&M University, 1978–1984
5. Graduate School Faculty, Texas A&M University , 1980–1984
6. Medical School Faculty, Meharry Medical College, 1984–1990
7. Faculty, School of Graduate Studies, Meharry Medical College, 1984–1990
8. School of Medicine, University of North Dakota, 1991–present
9. Graduate School Faculty, UND, 1991–present

Funded Grants

1. Scott and White Clinic and Hospital Medical Research Funds. To: M.R. Smigel(PI), J.W. Wagner, and G.K. Rieke. Pharmacological manipulation of cerebral ischemia. $28,214. 1981–1982.
2. Scott and White Clinic and Hospital Medical Research Funds. To: M.R. Smigel(PI), D.E. Bowers, M.S. Cannon, G.K. Rieke, and J.W. Wagner. Age related changes in human cerebrum and associated microvasculature. $35,300. 1981–1983.
3. Center for Comparative Medicine, Texas A&M University. Competitive peer reviewed grant. To: G.K. Rieke (PI) and J.F. Hunter. Do derivatives of pyrrolidine have a possible causal relationship to Huntington's disease? Electrophysiological, histological and behavioral tests of four pyrrolidine derivatives in a mouse model of Huntington's disease. $18,445. 1981–1982.
4. Center for Comparative Medicine, Texas A&M University. Competitive peer reviewed grant. To: G.K. Rieke (PI), J.F. Hunter, E.L. Mancall, J. Efimenko, and J.W. Wagner. Huntington's disease, L-pyroglutamic acid and closely related imino acids: evaluation of the role of L-pyroglutamate in HD in man and the mouse model. $18,445. 1982–1983.
5. Biomedical Research Support Grant, College of Medicine, Texas A&M University. To: G.K. Rieke(PI), A.D. Scarfe, J. Efimenko, and R. Storts. The role of L-pyroglutamate (L-PGA) in Huntington's disease and the chronic effects of L-PGA in the HD-rodent model. $4,500. 4/1/83–3/31/84.
6. NIH Division of Research Resources, Grant #1-G12-RR03032-01. "Research infrastructure for scientific excellence", Research Centers in Minority Institutions (RCMI). Dr. David Satcher (PI) $3,425,000. 1985-1990. To: G.K. Rieke as a member of the Neuroscience Component of the grant. $15,000. 1985–1986.
7. NSF, Behavioral and Neural Sciences, Molecular and Cellular Neurobiology. "Are Oligodendroglia Destroyed By L-Pyroglutamate Or Thyrotropin Releasing Hormone?" To: G.K. Rieke (PI). $20,000. BNS 8710184. 10/1/87–3/31/89.
8. NIH MBRS, DRR Scientific subproject, Minority Biomedical Research Support Grant. "Huntington's disease and the toxic metabolite L-pyroglutamate: Relationship?" To: G.K. Rieke (PI) $256,000. 1987–1991.
9. NSF, RIMI Program, Division of Research Initiation and Improvement. "Core Neurohistological and Radioimmunoassay Laboratories." PIs James G. Townsel, Linda D. Sanders, G.K. Rieke and William E. Thomas. $298,000. starting date 10/1/87, expires 9/30/90. The funds are for operating the two service laboratories.
10. . NSF-MRCE. Mechanisms of kainic acid neurotoxicity. G.K. Rieke and S.M. Fredman. Seed Grant. $6940. 1989–1990.
11. BRSG, UND School of Medicine. Testing an immunological method to uncouple striatal compartments by selective destruction of striatal interneurons. To: G.K. Rieke, $5058, Jan 1, 1993–Sept 31, 1994.
12. BRSG, UND School of Medicine. Striatal interneurons: connections defined by transneuronal C-fragment tetanus toxin tracer and double immunocytochemistry. A correlative light and electron microscopic study. To: G.K. Rieke and W.C. Perryman. Funded for $2500. Jan 1, 1994–September 30, 1994.
13. Faculty Research Grant (UND), Does the -amyloid protein fragment (AB1-42) kill cholinergic neurons in Alzheimer's disease? To: G.K. Rieke, Funded 2/95 to 1/96. $2500.
14. UND SoM Grant. Are forebrain cholinergic neurons destroyed by chronic challenge with the AB1-42 amyloid fragment? Funded 1/95–9/30/95. $2500. Garl K. Rieke.
15. Is AB1-42 Neurotoxicity Codependent on Activation of NMDA Receprors? In Vivo Effects of AP-5 and Mg⁺². UNDSoM Research Grant, $3750, March 1, 1996 to November 1, 1996. Garl K. Rieke.
16. Faculty Research and Creative Activity Grant (UND). Intracellular localization of site of synthesis of the neurotoxic fragment (AB1-42) of the Alzheimer precursor protein by electron microscopic-immunogold. To: G.K. Rieke, Funded $1997, (Nov. 1, 1996–Oct. 31, 1997). Extended to Nov. 1, 1998 because of the flood in Grand Forks, ND.
17. Neuropsychiatric Research Institute Small Grant Program. In situ ultrastructural identification of organelles immunoreactive to anti-amyloid beta protein fragment AB1-42 by EM immunogold. To: G.K. Rieke, (Asked for two years funding $6747) Funded $4000. 12/2/98 to 11/30/99.
18. UNDSMHS Research Grant. Ultrastructural identification of organelles immunoreactive to AB1-42 by EM-immunogold. To: G.K. Rieke, Funded $4969, March 1, 1999–November 1, 1999.
19. UND Senate Scholarly Activities Committee Research Grant. Localizing both “the cook” and its “deadly product” in the cellular kitchen. Garl K. Rieke. $1200, Nov/2000 to Feb/2001.
20. UND Senate Scholarly Activities Committee Research Grant. Do barrel like channels composed of amyloid beta proteins exist in membranes within nerve cells? Potential role in cell death and Alzheimer’s Disease. Garl K. Rieke. $2500 for one year through February 28, 2004.

Current Funding

1. Woodburne, L.S. and G.K. Rieke. Responses to symbols by squirrel monkies. Psychon. Sci., 5:429–430, 1966.
2. Rieke, G.K. and B.M. Wenzel. The ipsilateral olfactory projection field in the pigeon. In: D. Denton and J.P. Coghlan (eds.), Olfaction and Taste V, Academic Press, 1975, pp. 361–368.
3. Rieke, G.K. and B.M. Wenzel. Forebrain projections of the pigeon olfactory bulb. J. Morphology, 158:41–55, 1978.
4. Rieke, G.K. An inexpensive hydraulic micro-drive for recording single nerve cell activity. Review of Scientific Instruments, 50:637–640, 1979.
5. Rieke, G.K. Kainic acid lesions of the pigeon paleostriatum: A model for study of movement disorders. Physiol. & Behav., 24:683–687, 1980.
6. Bowers, D.E., G.K. Rieke and M.S. Cannon. Mast cells in the pigeon olfactory bulb. Avian Dis., 25:136–150, 1981.
7. Rieke, G.K. Movement disorders and lesions of pigeon brain stem analogues of basal ganglia. Physiol. & Behav., 26:379–384, 1981.
8. Rieke, G.K. and D.E. Bowers. Necrotizing effects of kainic acid on neurons in the pigeon brain: Histological observations. Brain Res., 212:411–423, 1981.
9. Rieke, G.K., D.E. Bowers and N.J. Silvy. A technique for improved fixation of the pigeon central nervous system for electron microscopy. Anat. Rec., 200:121–125, 1981.
10. Rieke, G.K., D.E. Bowers and P. Penn. The vascular pattern to the caudatoputamen and globus pallidus of rat: A scanning electron microscopic study of vascular endocasts of stroke prone vessels. Stroke, 12:840–847, 1981.
11. Rieke, G.K. and D.E. Bowers. Acute effects of the neurotoxin kainic acid on neurons of the pigeon basal ganglia: Electrophysiological and light and electron microscopic observations. Acta Neuropath. 56:123–135, 1982.
12. Rieke, G.K. The TPc, the avian substantia nigra: pharmacology and behavior. Physiol. & Behav., 28:755–763, 1982.
13. Rieke, G.K., A.D. Scarfe and J.F. Hunter. L-Pyroglutamate: An alternate neurotoxin for a rodent model of Huntington's disease. Brain Res. Bull., 13:443–456, 1984.
14. Rieke, G.K. and M.S. Cannon. A histochemical study of cerebral cortical vessels and ganglionic vessels of the caudatoputamen in aging normotensive male rats. Stroke, 16:285–292, 1985.
15. Scarfe, A.D., C.W. Steele and G.K. Rieke. Quantitative chemobehavior of fish: an improved methodology. Enviorn. Biol. Fish, 13:183–194, 1985.
16. Rieke, G.K. The thalamic arterial pattern: An endocast and scanning electron microscopic study in normotensive male rats. Amer. J. Anat., 178:45–54, 1987
17. Jordan, F.L., G.K. Rieke, and W.H. Thomas. Presence and development of ependymal cells in primary tissue cultures derived from embryonic rat cerebral cortex. Dev. Brain Res., 35:97–110, 1987.
18. Rieke, G.K., F.L. Jordan, H.J. Wynder, and W.E. Thomas. Ultrastructure of ependymal cells in primary cultures of cerebral cortex. J. Neurosci. Res., 18:484–492, 1987.
19. Rieke, G.K., H.W. Sampson, A.D. Scarfe, and D.E. Bowers. The toxin kainic acid: A study of avian nerve and glial cell responses utilizing tritiated kainic acid and electron microscopic autoradiography. Acta Neuropath., 76:185–203, 1988.
20. Rieke, G.K., J. Smith, O.B. Idusuyi, J. Semenya, R. Howard, and S. Williams. Chronic intrastriatal L-pyroglutamate: Neuropathology and neuron sparing like Huntington's disease. Exp. Neurol., 104:147–154, 1989.
21. Jordan, F.L., G.K. Rieke, B.W. Hughes, W.E. Thomas. Morphological diversity of ependymal cells in tissue culture. Brain Res Bull., 25:159–163, 1990.
22. Rieke, G.K. Chronic intrastriatal injection of the excitatory amino acid receptor antagonist L-Kynurenic acid, produces selective neuron sparing lesions as seen in Huntington's disease. Exp. Neurol., 115:228–238, 1992.
23. Rieke, G.K., K. Splichal and S. Meyer. Intracellular AB1-42 is localized in the endoplasmic reticulum, the nucleus and on mitochondria affording the peptide opportunity to interact with membranes leading to apoptotic cell death. Neurobiology of Aging, 23: S519, 2002
24. G. Rieke and J. Swinscoe. Intracellular AB tetramer in the ER and M in a rat model and human AD: Multiple causes of death. In: Alzheimer’s Disease: New Advances, Editors Khalid Iqbal, Bengt Winblad and Jesus Avilia. Midimond International Proceedings, pp. 491–494, 2006.

Abstracts

1. Rieke, G.K. and M.H. Bennett. A corticomedial amygdalobulbar system in olfaction in the male rat. Soc. Neurosci. Abstr., 2nd annual meeting, Houston,
   pp. 214, 1972.
2. Rieke, G.K. and B.M Wenzel. Responses evoked in centers of the pigeon telencephalon following stimulation of the olfactory bulb. Anat. Rec., 175:424, 1973.
3. Rieke, G.K. and B.M. Wenzel. A neuroanatomical investigation of the olfactory projection field in the pigeon (Columba livia). Soc. Neurosci. Abstr., 3rd Annual Meeting, San Diego, pp. 177, 1973.
4. Rieke, G.K. and B.M. Wenzel. A neuroanatomical investigation of the contralateral component of the olfactory projection field in the pigeon (Columba livia). Anat. Rec., 178:447, 1974.
5. Rieke, G.K. Direct retino-hypothalamic projections in the pigeon (Columba livia): An electrophysiological and neuroanatomical study. Anat. Rec., 181:462, 1975.
6. Rieke, G.K. and J.P. Corey. Hippocampal formation responses to electrical stimulation of the olfactory bulb and tract in the squirrel monkey. Soc. Neurosci. Abstr., 5th Annual Meeting, New York, pp. 537, 1975.
7. Rieke, G.K. Primate hippocampal formation responses to olfactory bulb or tract stimulation. Anat. Rec., 184:514, 1976.
8. Rieke, G.K. Olfactory evoked responses and induced seizures activity in the primate hippocampal formation. Soc. Neurosci. Abstr., 6th Annual Meeting, pp. 395, 1976.
9. Rieke, G.K. Field potentials in the olfactory produced by the action of centrifugal fiber systems upom the granule cells. Anat. Rec., 187:694–695, 1977.
10. Rieke, G.K. and J.P. Corey. Field potentials from the olfactory bulb by stimulation of selected centrifugal fiber systems. Anat. Rec., 190:522, 1978.
11. Corey, J.P. and G.K. Rieke. Effects of kainic acid on the neurons receiving olfactory nerve fibers in the rat olfactory bulb. Soc. Neurosci. Abstr., 8th Annual Meeting, St. Louis, pp. 442, 1978.
12. Rieke, G.K., D.E. Bowers, and M.S. Cannon. Putative tissue basophil/mast cell: A resident of the pigeon olfactory bulb. Soc. Neurosci. Abstr., 9th Annual Meeting, Atlanta, pp. 432, 1979.
13. Rieke, G.K. Kainic acid lesions of the pigeon paleostriatal complex: A model for the study of movement disorders. Anat. Rec., 196:157, 1980.
14. Rieke, G.K. Movement disorders associated with kainic acid lesions in parts of the avian "basal ganglia". Soc. Neurosci. Abstr., 6:809, 1980.
15. Bowers, D.E., H.W. Sampson, and G.K. Rieke. Ultrastructural changes in the kidney and liver of hypertensive aged rats--A preliminary report. Anat. Rec., 199:34A, 1981.
16. Rieke, G.K. and D.E. Bowers. The vascular supply to the caudatoputamen (CP) and globus pallidus (GP) in aging, normotensive male rats: Scanning electron microscopic observations of vascular endocasts of stroke prone vessels. Anat. Rec., 199:212, 1981.
17. Rieke, G.K. and D.E. Bowers. Acute effects of the neurotoxin kainic acid on neurons of the pigeon basal ganglia: Behavioral, electrophysiological, light and electron microscopic observations. Soc. Neurosci. Abstr., 7:785, 1981.
18. Rieke, G.K. Electrophysiological, histological and behavioral tests of four pyrrolidine derivatives in a mouse model of Huntington's disease (HD). Anat. Rec., 202:158A, 1982.
19. Rieke, G.K. and J.F. Hunter. Huntington's disease and L-pyroglutamic acid: A behavioral, electrophysiological and morphological evaluation of the possible role of this imino acid in Huntington's disease. Soc. Neurosci. Abstr., 8:249, 1982.
20. Rieke, G.K., A.D. Scarfe, and J.F. Hunter. L-Pyroglutamic acid: A neurotoxic imino acid that produces a drug induced animal model of Huntington's disease and with a potential role in the etiology of Huntington's disease. Soc. Neurosci. Abstr., 9:269, 1983.
21. Scarfe, A.D., C.W. Steele and G.K. Rieke. Quantitative chemobehavior of fish. Biennial Conference on Ethology and Behavioral Ecology of Fishes. Normal, Illinois, May 10–12, 1984.
22. Rieke, G.K., A.D. Scarfe, M.S. Cannon, J.F. Hunter and E.L. Mancall. L-Pyroglutamic acid: a toxic amino acid that produces an animal model of Huntington's disease and with possible etiological significance in HD. Anat. Rec., 208:147A, 1984.
23. Rieke, G.K., M.S. Cannon and H. Williams. Huntington's disease, L-pyroglutamate, thyrotropin releasing hormone and metabolites: Is there a causal relationship? Soc. Neurosci. Abstr., 10:994, 1984.
24. Rieke, G.K. The arterial vascular pattern to the thalamus in normotensive rats. Anat. Rec., 214:109A, 1986.
25. Jordan, F.L., G.K. Rieke and W.E. Thomas. Presence and development of ependymal cells in primary tissue cultures derived from embryonic rat cerebral cortex. Anat. Rec., 218:46–47A, 1987.
26. Rieke, G.K., F.L. Jordan, H.J. Wynder and W.E. Thomas. Development and ultrastructure of ependymal cells from embryonic rat cerebral cortex in vitro. NIH Centennial MBRS-MARC Symposium, Washington D.C., October 1–4, 1987.
27. Wynder, H.J., G.K. Rieke, B.W. Hughes, F.L. Jordan and W.E. Thomas. A characterization of ependyma from embryonic rat cerebral cerebral cortex in vitro facilitated by a novel staining activity. Soc. Neurosci. Abstr., 13:1510, 1987.
28. Rieke, G.K. Are TRH and its metabolites neurotoxins? The Dedication Symposium and Open House, The Neuroscience Laboratories, Meharry Medical College, Nashville, TN., May 14–15, 1987.
29. Rieke, G.K. and W.E. Thomas. Are oligodendrocytes destroyed by kainic acid? Anat. Rec., 220:80A, 1988.
30. Smith, J., O.B. Idusuyi and G.K. Rieke. Chronic intrastriatal injections of L-pyroglutamate in rat produce a drug-induced lesion of the striatum that mimics the neuropathology of Huntington's disease. Program and Abstracts, 32nd Annual Meharry Student Research Day, March 30, 1988.
31. Rieke, G.K. and S.M. Fredman. Intracellular injection of kainic acid excites Aplysia neurons. Soc. Neurosci. Abstr., 14:792, 1988.
32. Rieke, G.K., J. Smith, O.B. Idusuyi and J. Semenya. Chronic intrastriatal injections of L-pyroglutamate in rat produce a drug-induced lesion of the striatum that mimics the neuropathology of Huntington's disease. Abstracts and Program, Seventh Annual Southeastern Regional Society for Neuroscience Meeting, Birmingham, Alabama, May 20–21, 1988.
33. Fredman, S.M. and G.K. Rieke. Behavioral, physiological and morphological effects of kainic acid on Aplysia. Coldspring Harbor Symposium,
    September, 1988.
34. Rieke, G.K. and J. Semenya*. Chronic intrastriatal injection of L-pyroglutamate in rat produces selective neuronal sparing lesions that resemble the neuropathology in Huntington's disease. Anat. Rec., 223:95A, 1989.
35. Rieke, G.K. and J. Semenya*. Chronic injections of L-pyroglutamate into rat striatum selectively spares aspiny II neurons: Neuropathology similar to Huntington's disease. Soc. Neurosci. Abstr.,15: 914, 1989.
36. Rieke, G.K. and B. Kurunwune. Is the excitatory amino acid receptor antagonist Kynurenic acid a neurotoxin? Anat. Rec., 226: 84A, 1990.
37. Rieke, G.K. The Kynurenines: Neurotoxins with a potential role in Huntington's disease. Soc. Neurosci. Abstr., 16, Part 2:1120, 1990.
38. Rieke, G.K. Are the kynurenines selective neurotoxins with a possible role in Huntington's disease Eleventh Annual Frank Low Research Day, UND Med. Ed. Center, Fargo, ND., May 3, 1991.
39. Rieke, G.K. Chronic intrastriatal application of kynurenines produce a pattern of nerve cell loss similar to Huntington's disease. Soc. Neurosci. Abstr., 17:786, 1991.
40. Rieke, G.K., and W.C. Perryman. The kynurenines are endogenous neurotoxins that spare selective populations of neurons in the rat striatum. Anat. Rec. (Supplement 1): 98, 1993.
41. Rieke, G.K., W.C. Perryman, S.M. Walker, and T. Menisher. Performance deficits in a delayed spatial orientation task in rats with chronic bilateral injection of quinolinic acid into the medial striatum. Soc. Neurosci. Abstr., 19:366, 1993.
42. Dauphinais, J. and G.K. Rieke. Are the cognitive and memory deficits in a delayed spatial orientation task attributable to striatal damage in the rat model of Huntington's disease? Abstracts 1993 NIGMS Minority Symposium, Nov. 3–5, 1993, Atlanta.
43. Rieke, Garl K. Can the cognitive and memory disturbances characteristic of Huntington's Disease be attributed to damage to the striatum Proceedings North Dakota Academy of Sciences 48:7, 1994.
44. Perryman*, W.C., and Garl K. Rieke. Afferent connections of the globus pallidus as defined by a retrograde, transsynaptic tracer. Soc. Neurosci. Abstr., 20:333, 1994.
45. Walker, S.M., W.C. Perryman, and G.K. Rieke. Intrastriatal injections of quinolinic acid show marked choline acetyl-transferase and NADPH-diaphorasecell loss. Soc. Neurosci. Abstr., 20:989, 1994.
46. Rieke, G.K. Are cholinergic neurons of the basal forebrain destroyed by chronic challenge with B-amyloid fragments. Abstr. 15th Annual Frank Low Research Day, UNDSMHS, April 7, 1995, p.16.
47. Perryman, W.C. and G.K. Rieke. Extrastriatal and intra-striatal connections as defined by retrograde tracers and applied immunocytochemistry. Abstr. 15th Annual Frank Low Research Day, UNDSMHS, April 7, 1995, p. 45.
48. Rieke, G.K. Are cholinergic neurons of the basal forebrain destroyed in vivo by chronic challenge with amyloid fragments (AB1-42) or (AB1-40)? Soc. Neurosci. Abstr., 21:474, 1995.
49. Rieke, G.K. and K. Jacobson. AB1-42 neurotoxicity and the influence of NMDA receptor antagonists. Soc. Neurosci. Abstr., 22: 197, 1996.
50. Rieke, G.K. and K.A. Jacobson. AB1-42 neurotoxicity and the influence of NMDA receptor antagonists. Abstr. 17th Annual Frank Low Research Day: UNDSMHS, page 18, April 11, 1997.
51. Ruit K.G. and G.K. Rieke. Student performance and preference related to the implementation of "patient centered learning' and computer/video technology in a medical neuroscience curriculum. Abstr. 17th Annual Frank Low Research Day: UNDSMHS, page 19, April 11, 1997.
52. Jacobson, K.A., J.D. Berka and G.K. Rieke. Neurotoxic mechanism of the amyloid beta peptide (AB1-42) possible relevance to Alzheimer's disease. North Dakota Science, Engineering & Mathematics Poster Session, Abstr # 49, July 30, 1997, NDSU, Fargo, ND.
53. Rieke, G.K. and Katie A. Jacobson. Neurotoxic mechanisms of Alzheimer's AB1-42 protein fragment. Proceedings of the North Dakota Academy of Science, 51: 216, 1997.
54. Rieke, G.K. and Katie Jacobson. Localization of intracellular beta amyloid fragment in organelles by electron microscopic immunogold. Abstr. 18th Annual Frank Low Research Day: April 3, 1998.
55. Rieke, G.K., K. Jacobson, J.T. McCormack, and J. Rada. Intracellular localization of AB1-42 in the rat hippocampal neurons in vivo following challenge with 60 M chloroquine: A light and electrom microscopic immunogold study.
    Soc. Neurosci. Abstr. 24(1): 723, 1998.
56. Rieke, G.K. and Katie Jacobson. Localization of intracellular beta amyloid fragment in organelles by electron microscopic immunogold. North Dakota Science, Engineering and Mathematics, 6th Annual Poster Session Program, ND EPSCoR, NDSU, Fargo, ND. July 27, 1998.
57. Rieke, G.K., J.J. Spah, K.C. Jacobson, K. Wilson, J.T. McCormack and J. Rada. The Alzheimer’s amyloid beta fragment (AB1-42) appears within nerve cells: Implications regarding neurotoxicity. Abstr. 19th Annual Frank Low Research Day, UNDSMHS, April 9, 1999.
58. Andersen, J., J. Spah, K. Wilson and G.K. Rieke. The neurotoxic Alzheimer’s beta amyloid fragment (A42) is localized to nuclei, endoplasmic reticulum and mitochondria within neurons by electron microscopic immunogold in the chloroquine-induced rat model of Alzheimer’s disease. North Dakota Science, Engineering and Mathematics, 7th Annual Poster Session Program, NDEPSCoR, NDSU, Fargo, ND, July 28, 1999.
59. Andersen, J., J. Spah, K. Wilson and G.K. Rieke. The neurotoxic Alzheimer's beta amyloid fragment (A42) is localized to nuclei, endoplasmic reticulum and mitochondria within neurons by electron microscopic immunogold in the chloroquine-induced rat model of Alzheimer’s disease. The Second Regional North Dakota and South Dakota EPSCoR Program Meeting, NDSU, Fargo, ND., September 10, 1999.
60. Spah, J., K. Splichal, K. Wilson and G.K. Rieke. Beta Amyloid: The peptide that kills from both the outside and inside to produce Alzheimer’s Disease. Abstr 20th Annual Frank Low Research Day, UNDSMHS, April 7, 2000.
61. Spah, Jason, Katherine Splichal, Kali Wilson and Garl K. Rieke. Beta Amyloid: The peptide that kills from both the outside and inside to produce Alzheimer’s Disease. Proc. North Dakota Academy of Science, 54: 17, 2000. (April 28, 2000).
62. Rieke*, G.K., J. Spah, K. Splichal and K. Wilson. Beta Amyloid: The peptide that kills from both the outside and inside to produce Alzheimer’s Disease. Abstr. Soc. Neurosci., 26:1784, 2000.
63. Spah, J., K. Splichal, K. Wilson and G.K. Rieke. Beta amyloid: the peptide that kills from both the outside and inside to produce Alzheimer’s Disease. UNDSOMHS Basic Science Retreat, Frostfire Ski Resort, Walhalla, ND, May 19–21, 2000.
64. Spah, J., K. Splichal, K. Wilson and Dr. G.K. Rieke. The beta amyloid fragment (A42) is localized to endoplasmic reticulum, nuclei and mitochondria within neurons and kills neurons by inducing a cascade of intracellular proteins leading to apoptosis and Alzheimer's disease. North Dakota Science, Engineering and Mathematics 8th Annual Poster Session Program. UND, July 27, 2000.
65. Spah, K. Splichal, K. Wilson and G.K. Rieke. Beta amyloid: the peptide that kills from both the outside and inside to produce Alzheimer’s disease. Basic Science Retreat, Frostfire Mountain, Walhalla, ND. October 1–14, 2000.
66. G.K. Rieke, K. Splichal, C. Remboldt and S. Meyer. Intracellular A42 is localized in the endoplasmic reticulum and interacts with membrane lipids producing
    4-hydroxynonenal. Abstr. Soc. Neurosci., 27: 1141, 2001.
67. G.K. Rieke, K. Splichal, C. Remboldt and S. Meyer. Beta amyloid: the peptide that kills from both the outside and inside to produce Alzheimer’s Disease. Basic Science Graduate Retreat, Frostfire Mountain, Walhalla, ND.,
    October 12–14, 2001
68. Splichal, K., C. Remboldt and G.K. Rieke. Intracellular A42 interacts with the endoplasmic reticulum and mitochondria inducing a cascade of events leading to apoptosis and Alzheimer’s Disease. NDEPSCoR : North Dakota Science, Engineering and Mathematics, 9th Annual Poster Session Program (page 15, poster # 52), at North Dakota State University, Fargo, ND. July 25, 2001.
69. Splichal, K., S. Meyer and G.K. Rieke. The amyloid beta fragment (A1-42) is an intra- cellular protein with a probable causative role in Alzheimer’s disease. NDEPSCoR: North Dakota Science, Engineering and Mathematics, 10th Annual Poster Session Program (page 16, poster #57) at the University of North Dakota, Grand Forks, ND, July 24, 2002.
70. Rieke, G.K., and J. Swinscoe. Are barrel-like channels formed by beta amyloid peptides in the endoplasmic reticulum? Potential role in the pathophysiology of Alzheimer’s Disease. Program No. 944.15. 2003 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience, 2003. Online
71. Splichal, Katherine M., Meyer, Shane M., and Rieke, Garl K., The Amyloid-Beta fragment (A1-42) is an Intracellular Protein with a Probable Causative Role in Alzheimer’s Disease. Proceedings 95th Annual Meeting North Dakota Academy of Science 57:2003 (March 27–28, 2003).
72. Rieke, G, J. Swinscoe, K. Mann, S. Meyer and K. Splichal. AB-tetramers in the endoplasmic reticulum in a rat model and human AD: Neurodegenerative consequences. Neurobiology of Aging 25: S415, 2004 (9th International Conference on Alzheimer’s Disease and Related Disorders, July 17–22, 2004, Philadelphia, PA).
73. K. Mann, S. Herner, K. Splichal, and G.K. Rieke, Ph.D. Intracellular AB: Harmful effects on mitochondria (M) and endoplasmic reticulum (ER). 12th Annual Science, Engineering and Mathematics Poster Session, NDEPSCoR. Tuesday, August 3, 2004, NDSU, Fargo, ND.
74. G. Rieke, J. Swinscoe, K.Mann, S.Meyer and K. Splichal. Aß-tetramers in the endoplasmic reticulum in a rat model and human AD: Neurodegenerative consequences. AND K. Mann, S. Herner, K. Splichal and G.K. Rieke. Intracellular AB: Harmful effects of mitochondria (M) and endoplasmic reticulum (ER). Both presented at the 21st Annual UND Department of Anatomy and Cell Biology and the University of Manitoba Department of Anatomy Exchange Day. Winnipeg, Manitoba Canada, September 18, 2004
75. Rieke, G., J. Swinscoe, K. Mann, S. Meyer and K. Splichal. Aß-tetramers in the endoplasmic reticulum in a rat model and human AD: Neurodegenerative consequences. Presented at the 22nd Annual UND Department of Anatomy & Cell Biology and the University of Manitoba Department of Anatomy Exchange Day, September 10, 2005, Grand Forks, ND.
76. G. Rieke and J. Swinscoe, Dept Anatomy and Cell Biol, SMHS, Univ North Dakota, Grand Forks, ND 58202-9037, USA :”Aß-tetramers in the endoplasmic reticulum (ER) and mitochondria (M) in a rat model and human AD: Multiple causes of death”. Xth International Conference on Alzheimer’s Disease and Related Disorders (Madrid, Spain, July 15–20, 2006)
77. Alzheimer’s & Dementia, The Journal of the Alzheimer’s Association. 2 (3):Suppl 1, S208–209, 2006.
78. Rieke, G. and J. Swinscoe. “Aß-tetramers in the endoplasmic reticulum (ER) and mitochondria (M) in a rat model and human AD: Multiple causes of death” 23rd Annual UND Department of Anatomy and Cell Biology and the University of Manitoba Department of Anatomy Exchange Day. Winnipeg, Manitoba Canada, September 9, 2006

Teaching Experiences

1. Graduate Student at LSU, Dept of Anatomy-Gross Anatomy, Medical Histology and Neuroscience. 1967–1970.
2. Hahnemann University-extensive teaching-Neuroanatomy Core (course coordinator), Med. Histology, Neurobiology Core 3, Neurosurgery and Neurology Residents. Neuroscience and Review, Nursing Anatomy and Physiology. 1973–1978
3. Texas A&M University, College of Medicine–Neuroanatomy (course coordinator, 1979–1984), and Med. Histology Lab 1978–1984.
4. Meharry Medical College- Neuroanatomy (Regular Medical Program)
   1984–1989.
5. Meharry Medical College- Neuroanatomy (Special Medical Program)
   1985–1989.
6. Meharry Medical College- Dental Neuroscience, 1984–1990.
7. Meharry Medical College- Neuroanatomy Course Coordinator for Regular Medical Program and Special Medical Program 1989–1990.
8. Coordinator for Medical Neurosciences, University of North Dakota School of Medicine, 1991–1998.
9. Focal Problems UND School of Medicine, 1991–1993
10. Graduate Neuroscience 522 (6 credit hours) in Fall Semester 1993, to Janis Neumann, a MS candidate in the College of Nursing, UND.
11. Coordinator for Anatomy and Cell Biology Seminar (505) Topic was "The Neurobiology of Alzheimer's Disease" (Spring 1997).
12. Cell and Molecular Biology (Anat 529)–3 lectures on structure and function of the plasma membrane (Spring 1998 and Spring 1999).
13. Facilitator in Block 3 of the Patient Centered Medical Curriculum at UNDSOMHS (January 7, 1999–March 5, 1999).
14. Facilitator and Lecturer in Block 4 of the Patient Centered Curriculum at UNDSOMHS, (March 22, 1999 – May 14, 1999).
15. Graduate Neuroscience 522, August 24, 1999– December 17, 1999.
16. Cellular and Molecular Foundations of Biomedical Science (BIMD 500), 6 lectures given (3 on the structure and function of the plasma membrane; 3 lectures on cytoskeleton, muscle contractility and cell motility (October 19th, 25th (2) and November 22nd (2) and 24th (1), 1999.
17. Facilitator Block 3 of Patient Centered Medical Curriculum at UNDSMHS, January 10, 2000–March 3, 2000.
18. Taught (lecture and lab) Block 4 of the Patient Centered Curriculum at UNDSMHS, March 20, 2000 to May 12, 2000.
19. Anatomy 590 (Readings in Anatomy) for Sandra Siegel (2 credit hours, Fall Semester, 2000)
20. Graduate Neuroscience 522 (Anatomy 522) 6 credit hours, Fall Semester, 2000 (7 students) & Graduate Neuroscience 522 (Anatomy 522) 6 credit hours, Fall Semester, 2003 (5 students).
21. Cellular and Molecular Foundations of Biomedical Science (BIMD 500) 3 lectures: one on membrane structure, muscle contractility and cytoskeketon. Fall Semester 2000–2004.
22. Facilitate in Block 2 of Patient Centered Curriculum (PCL) UNDSMHS. October–December, 2001–2007.
23. Taught (Lecture and Lab) and Facilitate in Block 4 of the PCL Curriculum at UNDSOMHS 2001–2007 (12–1 lectures, 11 labs and 8 PCL cases/session).
24. Graduate Neuroscience (Anatomy 522) Course Coordinator, 6 credit hours, Fall Semester 2005 (I gave 15 of the 36 lectures) (2 students).
25. Graduate Neuroscience (Anatomy 522) Course Coordinator, 6 credit hours, Fall Semester 2006 (I gave 14 lectures of the 36, ran all labs) (4 students).
26. Cellular and Molecular Foundations of Biomedical Sciences (BIMD 500). Fall Semester 2005; Fall semester 2006, (4 lectures and one problem solving session).