New treatment for Alzheimer's disease

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w Approach to Treating Alzheimer’s Disease

Researchers at Ulsan National Institute of Science and Technology (UNIST) in South Korea have introduced a new approach to treat Alzheimer's Disease.

Alzheimer's disease (AD) is one of the most common forms of dementia. In the search for new drugs for AD, the research team, led by Professor Mi Hee Lim of Natural Science at UNIST has developed a metal-based substance that works like a pair of genetic scissors to cut out amyloid-β (Aβ), the hallmark protein of AD. The study has been featured on the cover of the January 2017 issue of the Journal of the American Chemical Society (JACS) and has been also selected as a JACS Spotlight article. Alzheimer's disease is the sixth leading cause of death among in older adults. The exact causes of Alzheimer's disease are still unknown, but several factors are presumed to be causative agents. Among these, the aggregation of amyloid-β peptide (Aβ) has been implicated as a contributor to the formation of neuritic plaques, which are pathological hallmarks of Alzheimer's disease (AD). As therapeutics for AD, Professor Lim suggested a strategy that uses metal-based complexes for reducing the toxicity of the amyloid beta (Aβ). Although various metal complexes have been suggested as therapeutics for AD, none of them work effectively in vivo. The research team has found that they can hydrolyze amyloid-beta proteins using a crystal structure, called tetra-N methylated cyclam (TMC). Hydrolysis is the process that uses water molecules to split other molecules apart. The metal-mediated TMC structure uses the external water and cut off the binding of amyloid-beta protein effectively. In this study, the following four metals (cobalt, nickel, copper and zinc) were placed at the center of the TMC structure. When the double-layered cobalt was added to the center, the hydrolysis activity was at the highest. The research team reported that the cobalt-based metal complex (Co(II)(TMC)) had the potential to penetrate the blood brain barrier and the hydrolysis activity for nonamyloid protein was low. Moreover, the effects of this substance on the toxicity of amyloid-beta protein were also observed in living cell experiments. "This material has a high therapeutic potential in the treatment of Alzheimer's disease as it can penetrate the brain-vascular barrier and directly interact with the amyloid-beta protein in the brain," says Professor Lim. This study has also attracted attention by the editor of the Journal of the American Chemical Society. "Not only do they develop new materials, but they have been able to propose details of the working principles and experiments that support them," according to the editor. "As a scientist, this is such a great honor to know that our recent publication in JACS was highlighted in JACS Spotlights," says Professor Lim. "This means that our research has not only been recognized as an important research, but also has caused a stir in academia." This study has been conducted in collaboration with Professor Jaeheung Cho of Daegu Gyeongbuk Institute of Science and Technology (DGIST), Professor Kiyoung Park of Korea Advanced Institute of Science and Technology (KAIST), and Dr. Sun Hee Kim of Korea Basic Science Institute (KBSI). It has been also supporte by the National Research Foundation of Korea (NRF) and the Ministry of Science, ICT and Future Planning (MSIP).

Adding Second Drug No Help in Alzheimer's

Here is a great dementia resource for caregivers and healthcare professionals,

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Medpage Today

Action Points
In moderate-to-severe Alzheimer's disease, continuing treatment with donepezil, a cholinesterase inhibitor, had some benefits, but adding memantine (Namenda) did not.
Note that memantine yielded similar benefits compared with placebo but the combination of memantine and donepezil was no better than donepezil alone.

For patients with moderate-to-severe Alzheimer's disease, continuing treatment with donepezil -- a cholinesterase inhibitor -- has some benefits, but adding memantine (Namenda) does not, a randomized trial showed.

Compared with stopping donepezil, continuing treatment for a year resulted in significant improvements in cognition and performance of the activities of daily living (P<0.001 for both), according to Robert Howard, MD, of King's College London, and colleagues.

Memantine yielded similar benefits compared with placebo but the combination of memantine and donepezil was no better than donepezil alone, the researchers reported in the March 8 issue of the New England Journal of Medicine.

In an accompanying editorial, Lon Schneider, MD, of the University of Southern California in Los Angeles, said the results with donepezil in the trial may not apply to other cholinesterase inhibitors because of differences in pharmacokinetics and mechanisms of action.

"Nor should the ... results be interpreted as evidence of the efficacy of indefinite treatment with donepezil," he noted. "More research is needed to assess the long-term benefits, the potential for harm and physiological tolerance, and the safe discontinuation of cholinesterase inhibitors as Alzheimer's disease progresses."

Cholinesterase inhibitors -- including donepezil -- have shown some benefits in patients with mild-to-moderate Alzheimer's disease, although no treatments have been able to halt disease progression.

When the disease worsens, clinicians must make a decision about continuing treatment, which is complicated by a greater risk of adverse outcomes, the need for permanent pacemakers, and hip fractures when treatment is not stopped.

In the DOMINO study, Howard and colleagues evaluated the effects of continuing donepezil with or without the addition of memantine in 295 patients with moderate-to-severe Alzheimer's disease who had been treated with donepezil for at least three months.

The patients were living in the community and either had a live-in caregiver or someone who visited them at least once a day.

The researchers assigned the patients to one of four groups for one year:

Continue donepezil at a dose of 10 mg daily and start placebo memantine
Continue donepezil and start memantine at a dose increasing to 20 mg daily
Gradually discontinue donepezil and receive placebo donepezil and placebo memantine
Gradually discontinue donepezil, receive placebo donepezil, and start memantine
The coprimary outcomes of the trial were changes on the Standardized Mini-Mental State Examination (SMMSE) and on the caregiver-rated Bristol Activities of Daily Living Scale (BADLS). The minimum clinically important differences were defined as 1.4 points and 3.5 points, respectively.

Compared with patients who stopped donepezil, those who continued treatment scored 1.9 points better on the SMMSE and 3 points better on the BADLS. Only the difference on the SMMSE exceeded the minimum clinically important threshold.

In his editorial, Schneider said the 1.9-point difference "is potentially important because many of the patients were severely impaired, on the cusp for needing nursing home care, and slightly worse cognitive function could affect their ability to remain at home."

Compared with patients who received placebo memantine, those who started the drug scored 1.2 points better on the SMMSE and 1.5 points better on the BADLS (P≤0.02 for both), although both figures fell short of being clinically important.

Combining donepezil and memantine was not superior to donepezil alone.

"Although memantine appears to be helpful for the treatment of moderate-to-severe Alzheimer's disease when used alone or when replacing donepezil, the results of the DOMINO trial do not support the typical use in the U.S., and an FDA-approved use, as add-on therapy to established donepezil treatment," according to Schneider, who noted that the finding conflicts with a previous, shorter trial.

Howard and colleagues pointed out that neither donepezil nor memantine halted the overall loss of cognitive function and functional abilities.

Compared with the changes in patients who received placebo for both drugs, the gains seen in the SMMSE score with donepezil and memantine represented just 32% and 20%, respectively, of the total decline during the study. The figures for the BADLS scores were 23% and 11%, respectively.

There were 188 serious adverse events, but only six were considered possibly related to the study drugs. Rates did not differ between groups.

Mitochondria Could Be Target For Therapeutic Strategy For Alzheimer's Disease Patients

ScienceDaily
Science News
(Nov. 5, 2008) — A study in the Sept. 21 on-line edition of Nature Medicine describes the function and interaction of a critical molecule involved in cell death in Alzheimer’s disease patients.

These new findings reveal that blocking this molecule, called Cyclophilin D (CypD), and development of surrounding mitochondrial targets may be viable therapeutic strategies......read the whole story
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Can tomatoes carry the cure for Alzheimer’s?

Study shows how transgenic plants are used to produce a vaccine against Alzheimer’s disease

8 July 2008

The humble tomato could be a suitable carrier for an oral vaccine against Alzheimer’s disease, according to HyunSoon Kim from the Korea Research Institute of Bioscience and Biotechnology (KRIBB) in Korea and colleagues from Digital Biotech Inc. and the Department of Biological Science at Wonkwang University. Although their research1, just published online in Springer’s journal Biotechnology Letters, is still in the early stages, it is a promising first step towards finding an edible vaccine against the neurodegenerative disease.

Alzheimer’s disease is the most common cause of dementia and it progresses over a long period of time. It is thought to be caused by the accumulation of human beta-amyloid, a toxic insoluble fibrous protein in the brain, which leads to the death of neurons. Reducing the accumulation of beta-amyloid may inhibit the degeneration of the nervous system and therefore prevent or delay the onset of Alzheimer’s disease. One approach is to stimulate the immune system to reduce beta-amyloid in the brain.

Kim and colleagues’ aim was to develop a plant-derived vaccine against Alzheimer’s disease, since beta-amyloid is toxic to animal cells. Tomatoes are an attractive candidate as a vaccine carrier because they can be eaten without heat treatment, which reduces the risk of destroying the immune stimulation potential of the foreign protein. The researchers inserted the beta-amyloid gene into the tomato genome and measured the immune responses to the tomato-derived toxic protein in a group of 15-month-old mice.

They immunized the mice orally with the transgenic tomato plants once a week for three weeks, and also gave the mice a booster seven weeks after the first tomato feed. Blood analyses showed a strong immune response after the booster, with the production of antibodies to the human foreign protein.

The authors conclude: “Although we did not reveal a reduction of existing plaques in the brain of mice challenged with tomato-derived beta-amyloid…this study represents a unique approach in which transgenic plants expressing beta-amyloid protein are used to produce a vaccine.” The team is currently looking at strategies to increase the potency of the tomato-based vaccine, because fresh tomatoes contain only 0.7% protein and levels of foreign protein are even lower.

Reference

Youm JW, Jeon JH, Kim H, Kim YH, Ko K, Joung H, Kim HS (2008). Transgenic tomatoes expressing human beta-amyloid for use as a vaccine against Alzheimer’s disease. Biotechnology Letters (DOI 10.1007/s10529-008-9759-5). This research was supported by the Plant Diversity Research Center of the 21st Century Frontier R&D Program, Korea.

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Why laughter is so important for those with dementia

Laughter, the physical response to perceived humor, Those with dementia can still perceive humor. Laughter has demonstrated positive effects on physical and psychological well-being.Dementia folks have improved well being from laughter. Thus if someone with dementia thinks something is funny, he will laugh. What helps is to have a group leader or care giver start laughing about something and invite the dementia person(s) to join in. Often you will find that laughter is contageous. Studies that focus on effects of humor on health and well-being of older adults are scarce.

Laughter therapy is in for those with dementia

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Are Humor and Word-Play Lost Skillls for Those with Alzheimer's?

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Have you heard of laughter clubs ?

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