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Alzheimer’s Disease Conundrum – Are We Near the End of the Puzzle?

Posted in Advanced Drug Manufacturing Technology, Biological Networks, Gene Regulation and Evolution, Biomarkers & Medical Diagnostics, Cell Biology, Signaling & Cell Circuits, Cerebrovascular and Neurodegenerative Diseases, Chemical Genetics, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Genome Biology, Genomic Testing: Methodology for Diagnosis, Human Immune System in Health and in Disease, Innovations in Neurophysiology & Neuropsychology, International Global Work in Pharmaceutical, Medical Imaging Technology, Image Processing/Computing, MRI, CT, Nuclear Medicine, Ultra Sound, Molecular Genetics & Pharmaceutical, Pharmaceutical Industry Competitive Intelligence, Proteomics, Regulated Clinical Trials: Design, Methods, Components and IRB related issues, Technology Transfer: Biotech and Pharmaceutical, tagged Alois Alzheimer, Alzheimer, Alzheimer Disease, Alzheimers Disease, ApoE, BCHE brain imaging, Beta amyloid, biomarkers, cellular inflammatiory response, CLU, conitive loss, Decode Genetics, dementia, Icelanders, innovative applications, Kári Stefánsson, mapping, Massachusetts General Hospital, Picalm, plaque regression, Tau protein on March 9, 2013| 1 Comment »

Alzheimer’s Genomic Diagnosis and Treatment

Curator: Larry H Bernstein, MD, FCAP

 

Gene Mutation Protects Against Alzheimer’s

by Greg Miller on 11 July 2012
Brain preserver. A newly discovered gene mutation appears to protect against Alzheimer’s disease. Credit: Alzheimer’s Disease Education and Referral Center/NIA/NIH
http://news.sciencemag.org/sciencenow/2012/07/gene-mutation-protects-against-a.html

A rare mutation that alters a single letter of the genetic code protects people from the

• memory-robbing dementia of Alzheimer’s disease.

The DNA change may inhibit the buildup of β amyloid, the

• protein fragment that forms the hallmark plaques in the brains of Alzheimer’s patients.
• The mutation affects a gene called APP,
• which encodes a protein that gets broken down into pieces,
• including β amyloid.

Researchers previously identified more than 30 mutations to APP, none of them good. Several of these changes increase β amyloid formation and cause

•      a devastating inherited form of Alzheimer’s that afflicts people in their 30s and 40s—

•      much earlier than the far more common “late-onset” form of Alzheimer’s

• that typically strikes people their 70s and 80s.

The new mutation, discovered from whole-genome data from 1795 Icelanders for variations in APP that protect against Alzheimer’s, appears to do the opposite. The mutation interferes with one of the enzymes that breaks down the APP protein and causes a 40% reduction in β amyloid formation

New pharmacological strategies for treatment of Alzheimer’s disease: focus on disease modifying drugs.
Salomone S, Caraci F, Leggio GM, Fedotova J, Drago F.
University of Catania, Viale Andrea Doria 6, Catania, Italy.
Br J Clin Pharmacol. 2012 Apr;73(4):504-17. doi: 10.1111/j.1365-2125.2011.04134.x.

Current approved drug treatments for Alzheimer disease (AD) include

• cholinesterase inhibitors (donepezil, rivastigmine, galantamine) and the
• NMDA receptor antagonist memantine.

These drugs provide symptomatic relief but poorly affect the progression of the disease. Drug discovery has been directed, in the last 10 years, to develop ‘disease modifying drugs’ hopefully able to counteract the progression of AD. Because in a chronic, slow progressing pathological process, such as AD, an early start of treatment enhances the chance of success,

• it is crucial to have biomarkers for early detection of AD-related brain dysfunction,
  • usable before clinical onset.

Reliable early biomarkers need therefore to be prospectively tested for predictive accuracy,

• with specific cut off values validated in clinical practice.

Disease modifying drugs developed so far include drugs to

• reduce β amyloid (Aβ) production,
• drugs to prevent Aβ aggregation,
• drugs to promote Aβ clearance,
• drugs targeting tau phosphorylation and assembly

None of these drugs has demonstrated efficacy in phase 3 studies. The failure of clinical trials with disease modifying drugs raises a number of questions, spanning from

• methodological flaws to
• fundamental understanding of AD pathophysiology and biology.

Diagnostic criteria applicable to presymptomatic stages of AD have now been published.

These new criteria may impact on drug development, such that future trials on disease modifying drugs will include populations susceptible to AD, before clinical onset. http://www.ncbi.nlm.nih.gov/pubmed/22035455

Gene mutation defends against Alzheimer’s disease
Rare genetic variant suggests a cause and treatment for cognitive decline.
Ewen Callaway  11 July 2012
http://www.nature.com/news/gene-mutation-defends-against-alzheimer-s-disease-1.10984

J. NIETH/CORBIS
Almost 30 million people live with Alzheimer’s disease worldwide, a staggering health-care burden that is expected to quadruple by 2050. Yet doctors can offer no effective treatment, and scientists have been unable to pin down the underlying mechanism of the disease.
Research published this week offers some hope on both counts – few people carry a genetic mutation that naturally prevents them from developing the condition – 0.5% of Icelanders have a protective gene, as are 0.2–0.5% of Finns, Swedes and Norwegians. Icelanders who carry it have a 50% better chance of reaching age 85, are more than five times more likely to reach it 85 without Alzheimer’s.   The mutation seems to put a brake on the milder mental deterioration that most elderly people experience. Carriers are about 7.5 times more likely than non-carriers to reach the age of 85 without major cognitive decline, and perform better on the cognitive tests that are administered thrice yearly to Icelanders who live in nursing homes.
The discovery not only confirms the principal suspect that is responsible for Alzheimer’s, it also suggests that the disease could be

• an extreme form of the cognitive decline seen in many older people.

The mutation — the first ever found to protect against the disease — lies in a gene that produces

• amyloid-β precursor protein (APP),
• which has an unknown role in the brain

APP was discovered 25 years ago in patients with rare,

• inherited forms of Alzheimer’s that strike in middle age.
• In the brain, APP is broken down into a smaller molecule called amyloid-β.

Visible clumps, or plaques, of amyloid-β found in the autopsied brains of patients are a hallmark of Alzheimer’s.
Scientists have long debated whether the plaques are a cause of the neuro­degenerative condition

• or a consequence of other biochemical changes associated with the disease.

The latest finding supports other genetics studies blaming amyloid-β, according to Rudolph Tanzi, a neurologist at the Massachusetts General Hospital in Boston and a member of one of the four teams that discovered APP’s role in the 1980s.
If amyloid-β plaques were confirmed as the cause of Alzheimer’s, it would bolster efforts to develop drugs that block their formation, says Kári Stefánsson, chief executive of deCODE Genetics in Reykjavik, Iceland, who led the latest research. He and his team first discovered the mutation by comparing the complete genome sequences of 1,795 Icelanders with their medical histories. The researchers then studied the variant in nearly 400,000 more Scandinavians.
This suggests that Alzheimer’s disease and cognitive decline are two sides of the same coin, with a common cause — the build-up of amyloid-β plaques in the brain, something seen to a lesser degree in elderly people who do not develop full-blown Alzheimer’s. A drug that mimics the effects of the mutation, might slow cognitive decline as well as prevent Alzheimer’s.
Stefánsson and his team discovered that the mutation introduces a single amino-acid alteration to APP. This amino acid is close to the site where an enzyme called

• β-secretase 1 (BACE1) ordinarily snips APP into smaller amyloid-β chunks —
• and the alteration is enough to reduce the enzyme’s efficiency.

Stefánsson’s study suggests that blocking β-secretase from cleaving APP has the potential to prevent Alzheimer’s, but Philippe Amouyel, an epidemiologist at the Pasteur Institute in Lille, France, says “it is very difficult to identify the

• precise time when this amyloid toxic effect could still be modified”.

“If this effect needs to be blocked as early as possible in life to protect against Alzheimer’s disease, we will need to propose a new design for clinical trials” to identify an effective treatment.

The results demonstrate that whole-genome sequencing can uncover very rare mutations that might offer insight into common diseases.

• disease risk, may be determined by genetic variants that slightly tilt the odds of developing disease
• In this case a rare mutant may provide very key mechanistic insights into Alzheimer’s

Jonsson, T. et al. Nature     http://dx.doi.org/10.1038/nature11283 (2012).
Kang, J. et al. Nature 325, 733–736 (1987).
Goldgaber, D., Lerman, M. I., McBride, O. W., Saffiotti, U. & Gajdusek, D. C. Science 235, 877–880 (1987).

BHCE genetic data combined with brain imaging using agent florbetapir connects the BHCE gene to AD plaque buildup. BHCE is an enzyme that breaks down acetylcholine in the brain, which is depleted early in the disease and results in memory loss.   http://www.genengnews.com/

New Alzheimer’s Genes Found
Gigantic Scientific Effort Discovers Clues to Treatment, Diagnosis of Alzheimer’s Disease
By Daniel J. DeNoon
WebMD Health News Reviewed by Laura J. Martin, MD
http://www.webmd.com/alzheimers/news/20110403/new-alzheimers-genes-found

A massive scientific effort has found five new gene variants linked to Alzheimer’s disease. The undertaking involved analyzing the genomes of nearly 40,000 people with and without Alzheimer’s. This study was undertaken by two separate research consortiums in the U.S. and in Europe, which collaborated to confirm each other’s results.
Four genes had previously been linked to Alzheimer’s. Three of them affect only the risk of relatively rare forms of Alzheimer’s. The fourth is APOE, until now the only gene known to affect risk of the common, late-onset form of Alzheimer’s. Roughly 27% of Alzheimer’s disease can be attributed to the five new gene variants.  Even though Alzheimer’s is a very complex disease, the new findings represent a large chunk of Alzheimer’s risk, according to Margaret A. Pericak-Vance, PhD, of the U.S. consortium –

• 20% of the causal risk of Alzheimer’s disease and
• 32% of the genetic risk.

Alzheimer’s Tied to Mutation Harming Immune Response
By GINA KOLATA   Published: November 14, 2012  in NY Times
http://www.nytimes.com/2012/11/15/health/gene-mutation-that-hobbles-immune-response-is-linked-to-alzheimers.html?_r=0
Alzheimer’s researchers and drug companies have for years concentrated on one hallmark of Alzheimer’s disease: the production of toxic shards of a protein that accumulate in plaques on the brain.
Two groups of researchers working from entirely different starting points have converged on a mutated gene involved in another aspect of Alzheimer’s disease:

• the immune system’s role in protecting against the disease.

The mutation is suspected of interfering with

• the brain’s ability to prevent the buildup of plaque.

When the gene is not mutated, white blood cells in the brain spring into action,

• gobbling up and eliminating the plaque-forming toxic protein, beta amyloid.

As a result, Alzheimer’s can be staved off or averted.  People with the mutated gene have a threefold to fivefold increase in the likelihood of developing Alzheimer’s disease in old age.

Comparing Differences

Dr. Julie Williams’s, Cardiff, Wales (European team leader) report identified CLU and Picalm. A second study published in Nature Genetics, by Philippe Amouyel from Institut Pasteur de Lille in France, pinpointed CLU and CR1. The greatest inherited risk comes from the APOE gene, discovered in 1993 by a team led by Allen Roses, now director of the Deane Drug Discovery Institute at Duke UMC, in Durham, North Carolina.
The findings “are beginning to give us insight into the biology, but I don’t think you can expect treatments overnight,” Dr. Michael Owen (Cardiff, Wales) said. Instead, the genes will show a mosaic of risk, and “the key issue is what hand of cards you’re dealt,” he said.

Promise for Early Diagnosis
BHCE genetic data combined with brain imaging using agent florbetapir connects the BHCE gene to AD plaque buildup. BHCE is an enzyme that breaks down acetylcholine in the brain, which is depleted early in the disease and results in memory loss.

Dr. Bernstein’s comments:

1. There has been a long history of failure of drugs to slow down the progression of Alzheimer’s.  Regression of the plaques has not corresponded with retention of cognitive ability, which has been behind the arguments over beta amyloid or tau.
2. We now have two particularly interesting mutations –
   1. ApoE gene mutation that increases risk
   2. APP mutation that quite dramatically affects retention of cognition

Related articles

• Alzheimer’s Disease: Green Tea Extract Found To Interfere With The Formation Of Amyloid Plaques (medicalnewstoday.com)
• Aging Brain – The Specific Gene That Causes It (belmarrahealth.com)
• The Pathogenic Aβ43 Is Enriched in Familial and Sporadic Alzheimer Disease (plosone.org)
• Damaged blood vessels loaded with amyloid worsen cognitive impairment in Alzheimer’s disease (eurekalert.org)
• Major step toward an Alzheimer’s vaccine (nextbigfuture.com)
• Damaged blood vessels loaded with amyloid worsen cognitive impairment in Alzheimer’s disease (medicalxpress.com)
• Top Signs You are at Risk for Alzheimer’s (belmarrahealth.com)
• A Reliable Way to Detect Endogenous Murine β-Amyloid (plosone.org)

β-amyloid fibrils. (Photo credit: Wikipedia)

English: PET scan of a human brain with Alzheimer’s disease (Photo credit: Wikipedia)

Depiction of amyloid precursor protein processing, created by I. Peltan Ipeltan (Photo credit: Wikipedia)

English: Diagram of how microtubules desintegrate with Alzheimer’s disease Français : La protéine Tau dans un neurone sain et dans un neurone malade Español: Esquema que muestra cómo se desintegran los microtúbulos en la enfermedad de Alzheimer (Photo credit: Wikipedia)

English: Histopathogic image of senile plaques seen in the cerebral cortex in a patient with presenile onset of Alzheimer disease. Bowdian stain. The same case as shown in a file “Alzheimer_dementia_(1)_presenile_onset.jpg”. (Photo credit: Wikipedia)

 

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Sequencing the exomes of 1,100 patients with neurodegenerative and neuromuscular diseases: A consortium of 18 European and Australian institutions

Posted in Alzheimer's Disease, Biological Networks, Gene Regulation and Evolution, Biomarkers & Medical Diagnostics, Bone Disease and Musculoskeletal Disease, Cell Biology, Signaling & Cell Circuits, Cerebrovascular and Neurodegenerative Diseases, Chemical Genetics, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Genome Biology, Genomic Testing: Methodology for Diagnosis, Innovations in Neurophysiology & Neuropsychology, Medical and Population Genetics, Molecular Genetics & Pharmaceutical, tagged Agilent Technologies, Decode Genetics, European Union, Motor neurone disease, Neurology, Neuromuscular disease, University of Tübingen on December 3, 2012| 1 Comment »

Reporter: Aviva Lev-Ari, PhD, RN

With $15.5M Grant, EU Consortium to Sequence 1,100 Exomes to Develop Diagnostics for Neurologic Diseases

November 28, 2012

By Molika Ashford

A consortium of 18 European and Australian institutions and industry partners will spend five years sequencing the exomes of 1,100 patients with neurodegenerative and neuromuscular diseases to create diagnostic panels and uncover novel therapeutic targets.

The group, known as the Neuromics Consortium, is funded with €12 million ($15.5 million) under the European Union’s seventh framework program.

Headed by the University of Tübingen, the project will involve collaboration between 12 academic centers. Iceland’s Decode Genetics will do the sequencing and will support analysis and return of results to participants. The group also plans to work with Agilent Technologies to develop and validate targeted sequencing-based diagnostic panels for specific neurologic diseases, including ataxia/paraplegias, spinal muscular atrophies and lower motor neuron diseases, and neuromuscular diseases, according to Tübingen’s Holm Graessner, the manager of the consortium.

Graessner told Clinical Sequencing News in an email that the Neuromics Consortium hopes its work will yield better diagnostic panels that can increase the diagnosis rate for ten main neurodegenerative and neuromuscular disease types — including ataxia, spastic paraplegia, Huntington’s disease, muscular dystrophy and spinal muscular atrophy — as well as provide information on genes and pathways that could inform new treatments.

According to the consortium, 30 percent to 80 percent of patients with these diseases are still undiagnosed by current single-gene tests or gene panels, and cohorts for each individual disorder are small. By combining patient groups and data from many centers and looking for commonality between some of these diseases, the consortium hopes to create diagnostics that cover a greater range of causative mutations.

While each specific disorder the group will study is relatively rare, many have overlapping manifestations, which suggest similarities in disease pathways pointing to common therapeutic strategies, according to the group.

Graessner said that the project’s whole-exome sequencing component will take place mostly in the first two years. According to the consortium’s plan, Decode Genetics — which expanded last year from array-based SNP genotyping research to a next-gen sequencing approach (CSN 11/9/2011) — will use its Illumina HiSeqs to sequence at least 1,100 subjects. The group expects this to increase the percentage of disease genes known for some of the more heterogeneous diseases in the set from about 50 percent to 80 percent.

According to Graessner, RNA sequencing is also part of the plan, as well as proteomic and other ‘omic analyses, especially as the researchers move from sequencing toward diagnostic panel development and therapeutic target research.

“We plan to [do whole-exome sequencing for] 1,100 subjects for gene identification … equally distributed over 10 disease areas,” Graessner wrote. “[This] will be done mainly in the first two years. However, for some of the diseases, such as ataxia/paraplegias, we have diagnostic panels already and in that case we [will] do the panels first and send the still unclear families for WES or WGS,” he wrote.

Graessner said that the group is just now shipping its first sample package to Decode. When this is finished the group will hold a workshop to discuss and train all the participating academic centers in the use of the Decode database for analysis of the results.

He said the team plans to work with the Halo Genomics division of Agilent, to validate diagnostic panels for ataxia, spinal muscular atrophies, lower motor neuron disease, and neuromuscular diseases. Halo was acquired by Agilent last year, and had developed an enrichment technology dubbed HaloPlex that it said was especially suited for targeted gene panels less than one megabase in size (IS 12/6/2011).

The group’s bioinformatics partner, Ariadne Genomics, will also analyze data to support the diagnostics research, as well as research on potential novel therapeutic targets, according to Graessner.

In a document describing the project, the consortium wrote that at the end of the funding period, it expects “to have elucidated the genetic basis for [more than] 80 [percent] of investigated patient groups.”

According to the group, the new genes will be added to existing databases and used to develop the first overlapping gene panel that can be used to diagnose several of these individual diseases, “overcoming time consuming and costly single gene analysis.”

Molika Ashford is a GenomeWeb contributing editor and covers personalized medicine and molecular diagnostics. E-mail her here.

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http://www.genomeweb.com//node/1158076?hq_e=el&hq_m=1423834&hq_l=9&hq_v=e1df6f3681

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