Pilot drug studies

Older news items (pre-2010) brought over from the old website

Tarenflurbil fails clinical trial

In another example of a drug that worked in mice but failed to show a benefit for patients, a study has found that the drug tarenflurbil, which supposedly suppresses the accumulation of amyloid plaque—did not slow cognitive decline or loss of usual daily activities (and was moreover associated with adverse effects including anemia, pneumonia, and herpes zoster). Although the drug showed promise in a small clinical trial, the results were negative in this larger, randomized trial, involving 1684 patients with mild Alzheimer’s. It’s suggested that rather than focusing on Alzheimer's disease and its specific characteristics, we should see dementia as a confluence of three common disease processes—Alzheimer's disease, vascular brain injury, and Lewy body disease.

Jonsson, M., Edman, Å., Lind, K., Rolstad, S., Sjögren, M., & Wallin, A. (2009). Apathy is a prominent neuropsychiatric feature of radiological white-matter changes in patients with dementia. International Journal of Geriatric Psychiatry, 9999(9999), n/a. doi: 10.1002/gps.2379.

http://www.eurekalert.org/pub_releases/2009-12/ghcc-jet121109.php

Neurogenesis improved in Alzheimer mice

Studies of adult neurogenesis in genetically engineered mice have revealed two main reasons why amyloid-beta peptides and apolipoprotein E4 impair neurogenesis, and identified drug treatments that can fix it. The findings point to a deficit in GABAergic neurotransmission or an imbalance between GABAergic and glutamatergic neurotransmission as an important contributor to impaired neurogenesis in Alzheimer’s. While stem cell therapy for Alzheimer’s is still a long way off, these findings are a big step toward that goal.

Gang Li et al. 2009. GABAergic Interneuron Dysfunction Impairs Hippocampal Neurogenesis in Adult Apolipoprotein E4 Knockin Mice. Cell Stem Cell, 5 (6), 634-645.

Binggui Sun et al. 2009. Imbalance between GABAergic and Glutamatergic Transmission Impairs Adult Neurogenesis in an Animal Model of Alzheimer's Disease. Cell Stem Cell, 5 (6), 624-633.

http://www.eurekalert.org/pub_releases/2009-12/gi-gsi113009.php

Protein identified that counterbalances Alzheimer's proteins

A mouse study has revealed that a protein called Reelin may provide a new approach to tackling Alzheimer’s. Reelin activates and strengthens the response of the NMDA receptor, which plays an important role in coordinating chemical signals between adjacent nerve cells. In the presence of too much amyloid-beta protein (as occurs in an Alzheimer’s brain), the receptor migrates into the cell, reducing the cell's sensitivity to incoming signals. However, with strong concentrations of Reelin, the receptor remains active and the cell continues receiving normally. The findings also make a connection with ApoE4 — the receptor that binds to ApoE also binds to Reelin, and is part of the complex that controls the sensitivity of the NMDA receptors.

Durakoglugil, M. S., Chen, Y., White, C. L., Kavalali, E. T., & Herz, J. (2009). Reelin signaling antagonizes β-amyloid at the synapse. Proceedings of the National Academy of Sciences, 106(37), 15938-15943. doi: 10.1073/pnas.0908176106.

http://www.eurekalert.org/pub_releases/2009-10/usmc-nfa100609.php

Epilepsy drug may help Alzheimer's patients

A study involving genetically engineered mice has found that mice given the anti-seizure drug valproic acid soon after onset of the disease showed improved memory and reduced plaques. The acid worked by blocking the cascade of reactions that leads to beta-amyloid plaques. Valproic acid helped mice less as their disease progressed.

Qing, H. et al. 2008. Valproic acid inhibits Aβ production, neuritic plaque formation, and behavioral deficits in Alzheimer's disease mouse models. The Journal of Experimental Medicine, Published online October 27.

http://www.eurekalert.org/pub_releases/2008-10/rup-edm102008.php

New drug for Alzheimer’s

A pilot study of 321 people with mild and moderate Alzheimer's disease has found that those who took the new drug Rember for 50 weeks demonstrated a dramatically smaller reduction (81%) in mental decline compared with those on the placebo. Those on rember did not experience a significant decline in their mental function over 19 months, while those on a placebo got worse. Rember is the first drug to act on the tau protein. A "phase 3" trial is planned for next year, involving a larger group of people with the disease, and if that is successful, the drug could be available by 2012.

The findings were presented at the international conference on Alzheimer's disease in Chicago.

http://www.guardian.co.uk/science/2008/jul/30/medicalresearch.health

Early study reveals new drug could improve executive function in Alzheimer's patients

A trial of a new drug called PBT2 has been found to improve two indicators of executive function in patients with Alzheimer's disease, and reduces levels of amyloid β in the cerebrospinal fluid. There was no significant effect on memory, but this could be because memory functions deteriorate more slowly than executive ones during the early stage, making changes harder to detect in such a short study. The parent compound to PBT2 is clioquinol.

Lannfelt, L. et al. 2008. Safety, efficacy, and biomarker findings of PBT2 in targeting Aβ as a modifying therapy for Alzheimer's disease: a phase IIa, double-blind, randomised, placebo-controlled trial. The Lancet Neurology, 7 (9), 779-786.

http://www.eurekalert.org/pub_releases/2008-07/l-esr072808.php
http://www.eurekalert.org/pub_releases/2008-07/icl-adp072908.php

Dimebon significantly improves Alzheimer's symptoms

A study involving 183 Russian patients with mild-to-moderate Alzheimer’s has found that a drug previously used as an antihistamine (dimebon) significantly improved cognitive performance. Moreover, it demonstrated increasing benefits over 12 months, which no currently approved therapies do.

Doody, R.S. et al. 2008. Effect of dimebon on cognition, activities of daily living, behaviour, and global function in patients with mild-to-moderate Alzheimer's disease: a randomised, double-blind, placebo-controlled study. The Lancet, 372 (9634), 207-215.

http://www.eurekalert.org/pub_releases/2008-07/l-dsi071608.php

Tarenflurbil slows decline of mild Alzheimer's patients

A trial of 210 patients with mild to moderate Alzheimer’s has found that those with mild Alzheimer’s who received 800mg of tarenflurbil twice a day for a year experienced a rate of decline 46% lower than placebo patients in the activities of daily living scale, and a 36% reduction in the pace of decline in global function.  In those with moderate Alzheimer’s, neither 400mg or 800mg of tarenflurbil had a significant effect, and indeed impacted negatively on a third measure of global function. Patients with mild Alzheimer’s who took 800mg for 24 months had lower rates of decline for all three primary outcomes than those who took it for a shorter period.

Wilcock, G.K. et al. 2008. Efficacy and safety of tarenflurbil in mild to moderate Alzheimer's disease: a randomised phase II trial. Lancet Neurology, 7, 483-493.

http://www.eurekalert.org/pub_releases/2008-04/l-tsd042808.php

Potential new drug target identified

A mouse study has successfully reduced the production of beta-amyloid peptides, and improved memory. These peptides are produced when enzymes cut APP at two places, called the beta-secretase and gamma-secretase sites. Previous research has focused on a mutant beta-secretase sequence only seen in one extended family of patients, the so-called Swedish mutation. The new study identifies a different enzyme, called Cathepsin B (CatB), which works to cut the normal beta-secretase site in more than 99% of patients with Alzheimer’s. Two compounds that inhibit CatB were successfully tested, producing great improvement in memory, as well as reduced brain levels of beta amyloid.

Hook, V.Y.H., Kindy, M. & Hook, G. 2008. Inhibitors of Cathepsin B Improve Memory and Reduce β-Amyloid in Transgenic Alzheimer Disease Mice Expressing the Wild-type, but Not the Swedish Mutant, β-Secretase Site of the Amyloid Precursor Protein. Journal of Biological Chemistry, 283, 7745-7753.

http://www.eurekalert.org/pub_releases/2008-03/uoc--pad031108.php

PLMI factor in sleep disturbance for dementia patients

A study of 102 people diagnosed with both cognitive impairment and sleep disturbance (average nightly sleep of seven or less hours and daytime sleep of 30 minutes or longer) found that periodic leg movement disorder (a condition that causes people to jerk and kick their legs every 20 to 40 seconds during sleep) was predictive of reduced total sleep time in older adults with Alzheimer disease and related dementias. Given that sleep disturbance in persons with dementia is a highly prevalent and disabling symptom, and sedative-hypnotics are not recommended, this finding is important because it suggests treatment of periodic leg movements may be beneficial.

Richards, K.C. et al. 2008. Periodic Leg Movements Predict Total Sleep Time in Persons with Cognitive Impairment and Sleep Disturbance. SLEEP, 31(2), 224-230.

http://www.eurekalert.org/pub_releases/2008-02/aaos-ppt012808.php

Reduction of tau protein protects against Alzheimer’s

A study using genetically engineered mice has found that when tau protein was reduced their memory function was retained and they lived a normal lifespan, even though amyloid-beta levels weren’t affected. They were also made mice more resistant to epileptic seizures.

Roberson, E.D. et al. 2007. Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model. Science, 316 (5825), 750-754.

http://www.eurekalert.org/pub_releases/2007-05/gi-sin042707.php

Marijuana may slow progression of Alzheimer's disease

New evidence suggests that marijuana — which has strong anti-inflammatory effects — may contain compounds that slow the memory loss associated with Alzheimer's disease. Treatment with a synthetic compound similar to marijuana (WIN-55212-2) reduced inflammation in older rats and substantially improved their memories.

The researchers presented their findings October 18 at the annual Society for Neuroscience meeting in Atlanta.

http://www.eurekalert.org/pub_releases/2006-10/osu-lb101206.php
http://www.sciencedaily.com/releases/2006/10/061018151055.htm

New drug reduces plaque and tangles in Alzheimer's mice

Alzheimer's mice that received a compound known as AF267B for eight weeks performed significantly better on a spatial memory test than untreated mice did. A different memory test that involved associating a place with a shock was not affected. The drug was found to reduce plaques and tangles in the hippocampus but not in the amygdala. AF267B seems to work in part by enhancing the activity of receptors for the neurotransmitter acetylcholine, and boosting the levels of an enzyme called alpha secretase, which blocks the production of beta-amyloid proteins. Suppressing the M1 receptors worsened the condition and performance of Alzheimer’s mice, confirming the important role of M1 receptors in modulating the plaques and tangles characteristic of Alzheimer’s.

Caccamo, A. et al. 2006. M1 Receptors Play a Central Role in Modulating AD-like Pathology in Transgenic Mice. Neuron, 49, 671-682.

http://www.scientificamerican.com/article.cfm?id=drug-found-to-reverse-the

New compound stops brain cell degeneration in Alzheimer's disease

A new orally administered compound specifically targeted to suppress brain cell inflammation and neuron loss associated with Alzheimer's disease has been developed. The compound, MW01-5-188WH, is rapidly absorbed by the brain and is non-toxic. It selectively inhibits production of pro-inflammatory proteins called cytokines by glia, giving it relevance for several neurodegenerative disorders. The compound suppressed brain inflammation and neuron dysfunction in the hippocampus and protected against cognitive decline in genetically engineered mice. The compound also restored normal levels of markers of synaptic dysfunction in the hippocampus and attenuated Alzheimer's-like behavioral deficits. The compound represents a new approach to Alzheimer’s therapy.

Ranaivo, H.R., Craft, J.M., Hu, W., Guo, L., Wing, L.K., Van Eldik, L.J. & Watterson, D.M. 2006. Glia as a Therapeutic Target: Selective Suppression of Human Amyloid-Induced Upregulation of Brain Proinflammatory Cytokine Production Attenuates Neurodegeneration. Journal of Neuroscience, 26, 662-670.

http://www.eurekalert.org/pub_releases/2006-01/nu-ncs011906.php

Testosterone improves quality of life

A 24-week study involving 16 male patients diagnosed with mild Alzheimer disease and 22 healthy male controls found that Alzheimer’s patients who received daily testosterone treatment showed significant improvement on a quality-of-life instrument that encompasses memory, interpersonal relationships, physical health, energy, living situation and overall well-being, however improvement in memory or other cognitive skills using cognitive tests did not reach significance. Among healthy controls, those receiving testosterone showed a non-significant trend toward greater improvement in self-rated quality of life.

Lu, P.H. et al. 2006. Effects of Testosterone on Cognition and Mood in Male Patients With Mild Alzheimer Disease and Healthy Elderly Men. Archives of Neurology, 63.
Full text at http://archneur.ama-assn.org/cgi/content/full/63.2.nct50002v1

http://www.eurekalert.org/pub_releases/2005-12/uoc--apt120805.php

Natural compound from 'pond scum' shows potential activity against Alzheimer's

A compound isolated from a cyanobacterium, a type of blue-green algae (‘pond scum’) shows promise of becoming a natural drug candidate for fighting Alzheimer's. Nostocarboline (the newly isolated compound) is a potent inhibitor of cholinesterase, with a potency comparable to galanthamine.

Becher, P.G., Beuchat, J., Gademann, K. & Jüttner, F. 2005. Nostocarboline: Isolation and Synthesis of a New Cholinesterase Inhibitor from Nostoc 78-12A. Journal of Natural Product, 68(12), 1793–1795.

http://www.eurekalert.org/pub_releases/2005-12/acs-ncf122705.php

Gas-blockers might slow down Alzheimer's disease

Beta-amyloid is known to cause brain cells to make an inhibitor of an enzyme that triggers the production of nitric oxide (iNOS). This enzyme is normally turned on during infection and is needed to help immune cells destroy invading pathogens, but it is not normally found in the brain, where it may cause cellular damage that destroys neurons. Although it’s long been known that iNOS is present in the brain lesions of Alzheimer’s patients, it hasn’t been known whether its presence makes things worse. A new study has now shown that Alzheimer's-prone mice that lack iNOS live twice as long and develop fewer brain lesions than iNOS-expressing mice. The researchers suggest that iNOS inhibitors might turn out to be an effective in slowing the progression of Alzheimer's disease.

Nathan, C. et al. 2005. Protection from Alzheimer's-like disease in the mouse by genetic ablation of inducible nitric oxide synthase. Journal of Experimental Medicine, 202, 1163-1169.

http://www.eurekalert.org/pub_releases/2005-10/joem-gms102005.php

New memory drug works best in combination with older drug

An experimental drug – a compound known as SGS742 – has been successful in animal studies in improving memory, and is now in human clinical trials. The drug works by blocking certain chemicals that interfere with memory formation, thus enabling better acquisition and retention of new information. It alters the activity of gene control machinery that is important for memory consolidation. It was most effective when used in conjunction with Aricept, an established Alzheimer’s drug.

Helm, K.A., Haberman, R.P., Dean, S.L., Hoyt, E.C., Melcher, T., Lund, P.K. & Gallagher, M. 2005. GABAB receptor antagonist SGS742 improves spatial memory and reduces protein binding to the cAMP response element (CRE) in the hippocampus. Neuropharmacology, 48(7), 956-64.

http://www.eurekalert.org/pub_releases/2005-06/jhu-nmd060905.php

Chemical decoy shows promise for slowing Alzheimer's

A chemical polymer shows promise in cell culture studies of slowing Alzheimer’s by blocking the toxic brain proteins thought to cause the disease. The likely candidate for any drugs developed from this approach would be people at increased risk of Alzheimer’s, who haven’t yet developed signs of the disease.

Good, T. & Patel, D. 2005. BIOT 421 Development of biomimetic materials for Alzheimer's disease. Presented at 2:05 p.m., Thursday, March 17, at the Convention Center, Room 31A, during the "Tissue Engineering/Biomaterials" symposium at the 229th national meeting of the American Chemical Society.

http://www.eurekalert.org/pub_releases/2005-03/acs-ds030705.php

Antibody treatment partially reverses nerve damage in Alzheimer disease

A mouse study has had success in significantly decreasing structural nerve damage in the brains of mice with Alzheimer’s, by administering an beta amyloid antibody treatment to the brain surface.

Brendza, R.P. et al. 2005. Anti-Aß antibody treatment promotes the rapid recovery of amyloid-associated neuritic dystrophy in PDAPP transgenic mice.Journal of Clinical Investigation, 115, 428-433.

http://www.eurekalert.org/pub_releases/2005-01/joci-atp011305.php
http://news.bbc.co.uk/go/pr/fr/-/1/hi/health/4188677.stm

Rolipram - a potential new treatment

In a mouse study, a phosphodiesterase 4 inhibitor, rolipram, was found to improve memory in both long-term potential and contextual learning. Rolipram's protective effect is due to its ability to modify gene expression, making brain synapses more resistant to the insult caused by the accumulation of Ab. The beneficial effect of rolipram treatment was found to extend for at least 2 months after the end of one course of the treatment, and was more effective in the later stages of the disease.

Gong, B., Vitolo, O.V., Trinchese, F., Liu, S., Shelanski, M. & Arancio, O. 2004. Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment. Journal of Clinical Investigation, 114, 1624-1634.

http://www.eurekalert.org/pub_releases/2004-12/joci-r-a111804.php

Keeping blood pressure & cholesterol low may help some dementia patients more than Alzheimer's drugs

A comprehensive review of all recent medical studies on mixed dementia, vascular dementia and Alzheimer's suggests that efforts to treat cardiovascular risk factors, especially high blood pressure, may be more effective for many than memory drugs in protecting brain function.

Langa, K.M., Foster, N.L. & Larson, E.B. 2004. Mixed Dementia: Emerging Concepts and Therapeutic Implications. JAMA, 292, 2901-2908.

http://www.eurekalert.org/pub_releases/2004-12/uomh-thy120904.php

New type of Alzheimer's drug on trial

A clinical trial is commencing to test the effectiveness of a new type of drug, called Alzhemed, that attacks amyloid. The trial will last 18 months and will enroll about 950 Alzheimer's patients with a mild-to-moderate form of the disease, from centers around the United States and Canada. The drug actually physically combines with amyloid to prevent plaque formation, and is also expected to inhibit the inflammatory response associated with amyloid buildup in Alzheimer's.

http://www.eurekalert.org/pub_releases/2004-11/tju-jns110204.php

Blood pressure drugs may slow deterioration of Alzheimer's

A study involving 162 people in Japan living in long-term care facilities with mild to moderate Alzheimer's disease and high blood pressure has found that certain blood pressure drugs may slow the deterioration of Alzheimer's disease. The results, while interesting, will need to be replicated in carefully controlled, randomized, blinded studies.

Ohrui, T., Tomita, N., Sato-Nakagawa, T., Matsui, T., Maruyama, M., Niwa, K., Arai, H. & Sasaki, H. 2004. Effects of brain-penetrating ACE inhibitors on Alzheimer disease progression. Neurology, 63, 1324-1325.

http://www.eurekalert.org/pub_releases/2004-10/aaon-bpd100404.php

Anti-cholesterol drug treats Alzheimer's disease in mice

A drug that jams a key enzyme regulating cholesterol (CP-113,818) has been found to drastically reduce the levels of amyloid plaque in genetically engineered mice. The drug has not been tested in clinical trials, but another ACAT inhibitor, avasimibe, is now in final clinical trials as a treatment for vascular disease and atherosclerosis.

Hutter-Paier, B., Huttunen, H.J., Puglielli, L., Eckman, C.B., Kim, D.Y., Hofmeister, A., Moir, R.D., Domnitz, S.B., Frosch, M.P., Windisch, M. & Kovacs, D.M. 2004. The ACAT Inhibitor CP-113,818 Markedly Reduces Amyloid Pathology in a Mouse Model of Alzheimer's Disease. Neuron, 44 (2), 227–238.

http://www.eurekalert.org/pub_releases/2004-10/cp-adt101204.php

Protein found that dissolves amyloid fibers

Amyloid plaque is extremely tough — so tough researchers have been unable to find a means to attack them. A new study suggests that yeast may be the means. Oddly, the yeast protein seems to be involved both in making amyloid fibers, and in dissolving them. The yeast protein Sup35 sometimes forms amyloid fibers in yeast cells — this is part of the cell's normal biology, changing the types of proteins that the cell makes. Another protein — Hsp104 — appears to affect Sup35's ability to form amyloid fibers. When a yeast cell contained either high amounts of Hsp104 or none at all, amyloid fibers never formed. But when Hsp104 levels were small, the fibers flourished. In the latest study, researchers found that small amounts of Hsp104 catalyzed the formation of amyloid fibers, but large levels of the protein actually caused the fibers to dissolve. Interestingly, Hsp104 belongs to a class of proteins that sometimes are influenced by environmental factors.

Shorter, J., & Lindquist, S. (2004). Hsp104 Catalyzes Formation and Elimination of Self-Replicating Sup35 Prion Conformers. Science, 304(5678), 1793–1797. doi:10.1126/science.1098007

http://www.eurekalert.org/pub_releases/2004-05/wifb-rdp052004.php

Clioquinol slowed progression of cognitive decline in Alzheimer's patients

A new clinical trial has found that the drug Clioquinol slowed the progression of cognitive decline in a group of 36 patients with moderate to severe Alzheimer’s, over a period of 24 weeks. PBT-1 (Clioquinol) is a chemical that binds zinc and copper, and has been shown to lower the levels of beta-amyloid and the associated toxicity in the brains of transgenic mice used as a model of Alzheimer's disease.

Ritchie, C.W. et al. 2003. Metal-Protein Attenuation With Iodochlorhydroxyquin (Clioquinol) Targeting A β Amyloid Deposition and Toxicity in Alzheimer Disease: A Pilot Phase 2 Clinical Trial. Archives of Neurology, 60, 1685-1691.

http://www.eurekalert.org/pub_releases/2003-12/aaft-cto121503.php

Cancer drug may help against Alzheimer's too

The drug Gleevec, approved for treatment of chronic myelogenous leukemia (CML) over two years ago, has been found to reduce the level of beta-amyloid in immature rat neurons and cultured human cells. The drug also significantly reduced the levels of amyloid peptides in live guinea pigs (who have amyloid peptides comparable to those found in humans). While still preliminary, the work may indicate a new approach to treating Alzheimer’s.

Netzer, W.J. et al. 2003. Gleevec inhibits β-amyloid production but not Notch cleavage. PNAS, 100, 12444-12449.

http://www.scientificamerican.com/article.cfm?id=cancer-drug-may-help-figh

New Drug for Moderate-to-Severe Alzheimer's

Four drugs — donepezil, galantamine, rivastigmine, and tacrine — are approved for treatment of mild-to-moderate Alzheimer's disease in the U.S., but there are no approved treatments for severe AD. Now an industry-sponsored study has examined memantine for this use. The study involved 252 patients with moderate-to-severe AD, over a period of 28 weeks. Patients were evaluated on 7 tests of cognition, functional capacity, and behavior. Outcomes were significantly better with memantine than with placebo on 4 of these scales, and no significant adverse events were noted. It is not clear yet how clinically meaningful these small improvements are. Memantine has been approved for use in Europe.

Reisberg, B., Doody, R., Stöffler, A., Schmitt, F., Ferris, S. & Möbius, H.J. 2003. Memantine in moderate-to-severe Alzheimer's disease. New England Journal of Medicine, 348, 1333-41.

http://www.eurekalert.org/pub_releases/2003-04/nyum-dsp032603.php

DHEA supplement shows no effect on Alzheimer's

The supplement dehydroepiandrosterone, or DHEA, had no effect on Alzheimer's patients who took the supplement for six months. A transient benefit on cognitive performance occurred at three months, but was not statistically significant. Of the 58 people who started the study, 46 completed three months of treatment and 33 completed six months of treatment. The small size of the study and the high number of people who dropped out may limit the findings of the study.

Wolkowitz, O.M., Kramer, J.H., Reus, V.I., Costa, M.M., Yaffe, K., Walton, P., Raskind, M., Peskind, E., Newhouse, P., Sack, D., De Souza, E., Sadowsky, C., Roberts, E. & the DHEA-Alzheimer’s Disease Collaborative Research Group. 2003. DHEA treatment of Alzheimer’s disease: A randomized, double-blind, placebo-controlled study. Neurology, 60, 1071-1076.

http://www.eurekalert.org/pub_releases/2003-04/aaon-dss033103.php

Designer chemical offers Alzheimer's hope

Researchers at the University of Illinois at Chicago have designed and synthesized highly potent inhibitor compounds that could lead to an effective treatment for Alzheimer’s disease. In earlier work, the researchers had designed an inhibitor that blocks the action of one of two enzymes thought to be responsible for Alzheimer’s disease. This enzyme, called memapsin 2, is responsible for producing beta-amyloid, which forms the plaques so characteristic of Alzheimer’s disease. The inhibitor was reported in the Journal of the American Chemical Society last year and was shown to be effective in test tube experiments. However, while useful as a model, the inhibitor was too big to be effective in drug therapy. What is needed is a compound small enough to cross the blood-brain barrier. This latest paper reports on a new, smaller, generation of inhibitors designed and tested in the laboratory.

Golestani, N., Molko, N., Dehaene, S., LeBihan, D., & Pallier, C. (2007). Brain Structure Predicts the Learning of Foreign Speech Sounds. Cereb. Cortex, 17(3), 575–582. doi:10.1093/cercor/bhk001

http://www.eurekalert.org/pub_releases/2001-08/uoia-dco080201.php

Naturally occurring protein could slow Alzheimer's disease

A cholesterol-lowering protein produced by the body, Apolipoprotein A-1, might be able to slow the progression of Alzheimer's disease.
Everyone has some quantity of Apo-A, in their body. It is produced in the small intestine and the liver and is known to help prevent coronary heart disease. At normal levels, the protein clears cholesterol throughout the body, including in the brain. The scientists speculate that boosting Apo-A levels may also help clear beta amyloid, an important part of the Alzheimer's disease plaques that strangle normal brain cells. Further testing is needed to confirm the role of Apo-A in animals and its relation with Alzheimer's, before any human trials could begin.

Koldamova, R. P., Lefterov, I. M., Lefterova, M. I., & Lazo, J. S. (2001). Apolipoprotein A-I Directly Interacts with Amyloid Precursor Protein and Inhibits Aβ Aggregation and Toxicity†. Biochemistry, 40(12), 3553–3560. doi:10.1021/bi002186k

http://www.eurekalert.org/pub_releases/2001-04/ACS-Nopc-0104101.php

Why Vitamin E might slow the progress of Alzheimer's

A chemical called methionine (an amino acid found in beta-amyloid) may be the source of the toxic free radicals produced by the amyloid-beta peptide. Recent studies have demonstrated that higher than normal doses of vitamin E may slow the advance of Alzheimer's in some people with late stages of the disease. The current study provides a possible explanation for this link. Vitamin E, an antioxidant, appears to work by destroying free radicals (oxidants) produced by amyloid.

The study was presented at the 2000 International Chemical Congress of Pacific Basin Societies.

http://www.eurekalert.org/pub_releases/2000-12/ACS-Ript-1712100.php