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04/2016 journal articles

Editorials

ALZHEIMER’S ASSOCIATION: INITIATIVES & PUBLIC HEALTH PERSPECTIVE

H.M. Snyder, M.C. Carrillo

J Prev Alz Dis 2016;3(4):178-180

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An estimated 47 million people worldwide are living with dementia in 2015 and this number is expected to triple by 2050. There is a clear urgency for therapies and / or interventions to slow, stop or prevent dementia. Amounting evidence suggests strategies to reduce risk of development dementia may be of growing import for reducing the number of individuals affected. The Alzheimer’s Association believes, from a population based perspective that: (1) Regular physical activity and management of cardiovascular risk factors (e.g. diabetes, obesity, smoking and hypertension) have been shown to reduce the risk of cognitive decline and may reduce the risk of dementia; (2) A healthy diet and lifelong learning/cognitive training may also reduce the risk of cognitive decline. The current evidence underscores the need to communicate to the broader population what the science indicates and to do so with diverse stakeholders and consistent messaging. There has never been a better time to define and distribute global messaging on public health for dementia.

CITATION:
H.M. Snyder ; M.C. Carrillo (2016): Alzheimer’s Association: Initiatives and Public Health Perspective. The Journal of Prevention of Alzheimer’s Disease (JPAD). http://dx.doi.org/10.14283/jpad.2016.111

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AT A CROSSROADS: A PERSPECTIVE ON DRUG DEVELOPMENT FOR ALZHEIMER’S DISEASE IN 2016

D. Michelson, M.Egan

J Prev Alz Dis 2016;3(4):181-184

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CITATION:
D. Michelson ; M.Egan (2016): At a Crossroads: A Perspective on Drug Development for Alzheimer’s Disease in 2016. The Journal of Prevention of Alzheimer’s Disease (JPAD). http://dx.doi.org/10.14283/jpad.2016.106

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GLOBAL ALZHEIMER’S PLATFORM TRIAL READY COHORTS FOR THE PREVENTION OF ALZHEIMER’S DEMENTIA

R. Sperling, J. Cummings, M. Donohue, P. Aisen

J Prev Alz Dis 2016;3(4):185-187

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With the now widely accepted view that preventing Alzheimer’s disease likely will require treatment in the earliest stages of disease, a number of secondary prevention trials have been launched. Recruiting sufficient numbers of participants for these trials represents a major roadblock. To address this barrier, the Global Alzheimer’s Platform Trial Ready Cohorts for Preclinical and Prodromal Alzheimer’s Dementia (GAP TRC-PAD) has created an efficient and sustainable recruitment system for upcoming secondary prevention trials. The initial goal of this effort will be to identify a large number of potential participants, rapidly screen these individuals using an adaptive risk algorithm, and ultimately identify 1000 preclinical and 1000 prodromal participants for the first GAP clinical trials. Embedded in this effort will be the development and validation of web-based cognitive and functional assessments for use in future trials. In combination with other GAP infrastructure, this initiative will provide an integrated platform to support efficient clinical trials not only in the pre-dementia space, but across all disease stages

CITATION:
R. Sperling ; J. Cummings ; M. Donohue ; P. Aisen (2016): Global Alzheimer’s Platform Trial Ready Cohorts for the Prevention of Alzheimer’s Dementia. The Journal of Prevention of Alzheimer’s Disease (JPAD). http://dx.doi.org/10.14283/jpad.2016.108

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EFFECTS OF THE VACCINE VANUTIDE CRIDIFICAR WITH QS-21 ADJUVANT ON IMMUNOGENICITY

F. Jessen

J Prev Alz Dis 2016;3(4):188

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CITATION:
F. Jessen (2016): Effects of the Vaccine Vanutide Cridificar with QS-21 Adjuvant on Immunogenicity. The Journal of Prevention of Alzheimer’s Disease (JPAD). http://dx.doi.org/10.14283/jpad.2016.116

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Commentary

THE PARADOX OF RESEARCH ON DEMENTIA-ALZHEIMER’S DISEASE

Z.S. Khachaturian, A.S. Khachaturian

J Prev Alz Dis 2016;3(4):189-191

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CITATION:
Z.S. Khachaturian ; A.S. Khachaturian (2016): The Paradox of Research on Dementia-Alzheimer’s Disease. The Journal of Prevention of Alzheimer’s Disease (JPAD). http://dx.doi.org/10.14283/jpad.2016.117

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Original Research

A RANDOMIZED, DOUBLE-BLIND, PHASE 2 STUDY OF THE EFFECTS OF THE VACCINE VANUTIDE CRIDIFICAR WITH QS-21 ADJUVANT ON IMMUNOGENICITY, SAFETY AND AMYLOID IMAGING IN PATIENTS WITH MILD TO MODERATE ALZHEIMER’S DISEASE

N. Ketter, E. Liu, J. Di, L.S. Honig, M. Lu, G. Novak, J. Werth, G. LePrince Leterme, A. Shadman, H.R. Brashear

J Prev Alz Dis 2016;3(4):192-201

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Background: Vanutide Cridificar (ACC-001), a novel investigational immunotherapeutic vaccine designed to elicit antibodies against the N-terminal peptide 1-7 of the amyloid-beta peptide, believed to be important in the pathogenesis of Alzheimer’s disease (AD). Objectives: To evaluate the immunogenicity, safety and impact of ACC-001 with Quillaja saponaria (QS-21) adjuvant on the reduction of brain fibrillar amyloid burden, assayed by positron emission tomography (PET) imaging, in patients with mild to moderate AD. Design: Randomized, phase 2, interventional study. Trial registration: ClinicalTrials.gov Identifier: NCT01284387. Participants: Individuals with mild to moderate Alzheimer’s disease (Mini-Mental State Examination scores 18-26; measurable amyloid burden in the expected range, on the screening 18F-florbetapir PET scan; and a Rosen modified Hachinski ischemic score ≤4). Intervention: Participants were randomized to 3 μg or 10 μg ACC-001 (each in combination with 50 μg QS-21) or placebo (without QS-21). Measurements: Primary endpoint was the change from baseline to week 104 in cerebral amyloid burden as measured by the global cortical average (GCA) standard value uptake ratio (SUVR) based on the brain 18F-florbetapir PET composite cortical SUVR between each ACC-001+QS-21 dose compared with placebo. Secondary endpoints included safety, immunogenicity and pharmacodynamics. Exploratory endpoints included cognitive and functional efficacy, and health outcome measures. Results: Of 126 randomized patients (placebo: 40; ACC-001 3 µg+QS-21: 43; and ACC-001 10 µg+QS-21: 43), 125 received study treatment; 92 (73%) completed the study. Change in 18F-florbetapir PET GCA SUVR, was not significantly different between either of the two ACC-001+QS-21 treatment groups and placebo (3 μg +QS-21 vs. placebo diff=-0.03, p=0.54; 10 μg +QS-21 vs. placebo diff=-0.08, p=0.07), but the trend was numerically consistent with a dose response. The geometric mean peak anti-Aβ IgG titers were slightly higher in the 10 μg than the 3 μg group. The proportion of responders was similar in both dose groups of ACC-001+QS 21. The cerebrospinal fluid (CSF) p-tau changes from baseline in both active treatment groups were not statistically different from placebo, but were numerically consistent with a dose response (3 μg +QS-21 vs. placebo diff=-3.2, p=0.57; 10 μg +QS-21 vs. placebo diff=-7.0, p=0.19). The vMRI showed statistically significant faster treatment-related decrease in brain volume in the 10 μg group but was not significant in the 3 μg group, compared with placebo (3 μg diff =-1.3 mL/year, p=0.50; 10 μg diff=-4.2 mL/year, p=0.02). Measured plasma Aβ levels increased in parallel with peak anti-Aβ titers after each injection. Amyloid-related imaging abnormalities with edema/effusion (ARIA-E) were more frequent in patients who received ACC-001+QS-21 than placebo (6% vs. 0%) but none were symptomatic. The most common treatment-emergent adverse events in the active groups were injection reactions, and occurred more frequently in the ACC-001+QS-21 groups than the placebo (48% vs 8%), the majority of which were mild and transient. Conclusions: Primary biomarker efficacy endpoints were not statistically significant in either dose group. The numerical decreases in 18F-florbetapir PET GCA SUVR suggests a dose-related trend for greater reductions in fibrillar amyloid burden in the ACC-001+QS-21 10 ug group compared with placebo. Likewise, while not significant, there was a numerical trend of decreased CSF p-tau levels with ACC-001, possibly consistent with a downstream effect in the ACC 001+QS-21 group. Insufficient antibody titers or quality, insufficient power to detect a difference, or too short duration of follow up may be reasons why a statistically significant response was not observed. Brain volume measures showed faster volume loss in the 10 µg treatment group, similar to the effect seen in few earlier AD immunotherapy trials which may suggest removal of amyloid and resultant decrease in inflammation. No new, unexpected safety signals were detected.

CITATION:
N. Ketter ; E. Liu ; J. Di ; L.S. Honig ; M. Lu ; G. Novak ; J. Werth ; G. LePrince Leterme ; A. Shadman ; H.R. Brashear (2016): A Randomized, Double-Blind, Phase 2 Study of the Effects of the Vaccine Vanutide Cridificar with QS-21 Adjuvant on Immunogenicity, Safety and Amyloid Imaging in Patients with Mild to Moderate Alzheimer’s Disease. The Journal of Prevention of Alzheimer’s Disease (JPAD). http://dx.doi.org/10.14283/jpad.2016.118

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REVERSIBLE AND SPECIES-SPECIFIC DEPIGMENTATION EFFECTS OF AZD3293, A BACE INHIBITOR FOR THE TREATMENT OF ALZHEIMER’S DISEASE, ARE RELATED TO BACE2 INHIBITION AND CONFINED TO EPIDERMIS AND HAIR

G. Cebers, T. Lejeune, B. Attalla, M. Soderberg, R.C. Alexander, S. Budd Haeberlein, A.R. Kugler, E.W. Ingersoll, S. Platz, C.W. Scott

J Prev Alz Dis 2016;3(4):202-218

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Background: AZD3293 (also known as LY3314814) is a novel, potent, non-selective BACE1/BACE2 inhibitor currently in Phase 3 clinical development for the treatment of Alzheimer’s disease. Objectives: The purpose of these studies was to characterize the effects, putative mechanism, and reversibility of hypopigmentation following treatment with AZD3293 in pigmented Long-Evans rats, Beagle dogs, human cell cultures, and humans. Design: Nonclinical studies were conducted in Long-Evans pigmented rats, and both young and older Beagle dogs using a variety of oral dose levels of AZD3293 or AZD3839 (BACE inhibition reference compound; used in older dogs only) for dosing durations of 13 to 26 weeks. In vitro studies of normal human epidermal melanocytes and reconstituted human epidermis were also conducted. Skin biopsy data from a multiple-dose Phase 1 clinical study of AZD3293 (NCT01795339) are also reported. Setting: Nonclinical in vivo and in vitro studies were conducted in laboratory settings in the US, Canada, and France; the multiple dose clinical study was conducted in a specialized inpatient setting in the US. Participants: Beagle dogs: 13-week study N=36 young (8-10 mo) animals; 39-week study N=64 young animals; and a second 13-week study N=32 older (30-32 mo) animals. Long-Evans rats: N=68 animals. Multiple-dose clinical study: only data for subjects enrolled in Part 2 of this study are included in this report (N=16). Interventions: AZD3293 was the primary intervention used in these studies. AZD3839, a relatively BACE1-selective reference inhibitor compound was used in one group in the 13 week study in older Beagle dogs and one in vitro assessment. Finally, AZ1340, another relatively BACE1-selective reference inhibitor compound was used only in one in vitro assessment. Measurements: Measurements for the nonclinical studies in dogs and rats included macroscopic observation and assessment of skin biopsies via histopathology, immunochemistry, and electron microscopy. Measurements for the in vitro studies included melanocyte premelanosome protein (PMEL) processing, cytotoxicity, melanin synthesis, Pmel17 labeling, and melanocyte dendricity. Measurements in the clinical study included scoring of melanin content in skin biopsies taken before and after dosing with AZD3293 over 14 days at dose levels up to 150 mg. Results: Depigmentation in rats and dogs was limited to skin, hair, and mucosa with no effects on other pigmented tissues. At a cellular level depigmentation was observed within a week of treatment, whereas the appearance of depigmentation in skin and hair did not become apparent until, at earliest, 4 weeks of treatment. The depigmentation effects were reversible, not associated with degenerative or inflammatory changes, and were dose- and species-dependent in severity. Full recovery of melanization was observed at the microscopic (cellular) level and at least partial recovery was seen in the macroscopic appearance of animals by the end of the 12-week recovery period in both rats and dogs. Interestingly, no changes in melanin production or melanocyte morphology were seen in human primary melanocytes or reconstituted human epidermis in vitro. Finally, there were no changes in melanization level in skin biopsies following 12 days of daily AZD3293 treatment at doses of AZD3293 up to 150 mg/day in human subjects. Conclusions: AZD3293, a novel, potent, non-selective BACE1/BACE2 inhibitor is in development as a potentially disease-modifying treatment for Alzheimer’s disease. Chronic nonclinical studies in Beagle dogs and pigmented rats showed macroscopic and microscopic hypopigmentation effects of AZD3293 that were limited to skin, hair, and mucosa. These effects were shown to be reversible in both species. Analysis of data from nonclinical and in vitro studies suggests that hypopigmentation is caused by BACE2 inhibition resulting in accumulation of a premelanosome protein fragment, which interrupts the normal production of melanin. No macroscopic or microscopic reports of hypopigmentation were observed in a Phase 1 clinical study following 13 doses of AZD3293 over 14 days at dose levels up to 150 mg/day. These data suggest that hypopigmentation is species-specific and humans appear to be least sensitive to the depigmentation effect caused by BACE2 inhibition.

CITATION:
G. Cebers ; T. Lejeune ; B. Attalla ; M. Soderberg ; R.C. Alexander ; S. Budd Haeberlein ; A.R. Kugler ; E.W. Ingersoll ; S. Platz ; C.W. Scott (2016): Reversible and Species-Specific Depigmentation Effects of AZD3293, a BACE Inhibitor for the Treatment of Alzheimer’s Disease, Are Related to BACE2 Inhibition and Confined to Epidermis and Hair. The Journal of Prevention of Alzheimer’s Disease (JPAD). http://dx.doi.org/10.14283/jpad.2016.119

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CLINICAL BENEFITS OF TRAMIPROSATE IN ALZHEIMER’S DISEASE ARE ASSOCIATED WITH HIGHER NUMBER OF APOE4 ALLELES: THE “APOE4 GENE-DOSE EFFECT”

S. Abushakra, A. Porsteinsson, B.Vellas, J. Cummings, S. Gauthier, J.A. Hey, A. Power, S. Hendrix, P. Wang, L. Shen, J. Sampalis, M. Tolar

J Prev Alz Dis 2016;3(4):219-228

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Background: Tramiprosate is an oral amyloid anti-aggregation agent that reduces amyloid oligomer toxicity in preclinical studies and was evaluated in two 78-week trials in North America and Western Europe that enrolled 2,025 patients with Mild to Moderate Alzheimer’s Disease. The completed North American study did not achieve its efficacy objectives, but a pre-specified subgroup analysis suggested potential efficacy in apolipoprotein E4 (APOE4) carriers. To further explore this observation, we analyzed tramiprosate Phase 3 clinical data based on the number of APOE4 alleles. Objectives: To analyze tramiprosate efficacy, safety, and occurrence of vasogenic edema in the three APOE4 subgroups: homozygous, heterozygous and non-carriers. Design: Randomized, double-blind, placebo-controlled parallel-arm multi-center studies. Setting: Academic Alzheimer’s disease & dementia centers, community-based dementia and memory clinics, and neuropsychiatric clinical research sites. Participants: Subjects included 2,025 patients, 50 years of age or older, with approximately 60% having APOE4 carrier status (10-15% homozygotes and 45-50% heterozygotes), and mild to moderate disease. All subjects were on stable symptomatic drugs. Intervention: Randomized subjects received placebo, 100 mg BID, or 150 mg BID of tramiprosate. Measurements: Co-primary outcomes in both studies were change from baseline in the ADAS-cog11 and CDR-SB assessment scales. Results: Highest efficacy was observed in APOE4/4 homozygotes receiving 150 mg BID of tramiprosate, showing statistically significant effects on ADAS-cog and positive trends on CDR-SB (respectively, 40-66% and 25-45% benefit compared to placebo). APOE4 heterozygotes showed intermediate efficacy, and non-carriers showed no benefit. In 426 patients with MRI scans, no cases of treatment-emergent vasogenic edema were observed. In the three subgroups, the most common adverse events were nausea, vomiting, and decreased weight. Conclusions: The “APOE4 Gene-Dose effect” is likely explained by the high prevalence of amyloid pathology in symptomatic APOE4 carriers. In APOE4/4 Alzheimer’s disease patients, the high dose of tramiprosate showed favorable safety and clinically meaningful efficacy in addition to standard of care.

CITATION:
S. Abushakra ; A. Porsteinsson ; B.Vellas ; J. Cummings ; S. Gauthier ; J.A. Hey ; A. Power ; S. Hendrix ; P. Wang ; L. Shen ; J. Sampalis ; M. Tolar (2016): Clinical Benefits of Tramiprosate in Alzheimer’s Disease Are Associated with Higher Number of APOE4 Alleles: The “APOE4 Gene-Dose Effect”. The Journal of Prevention of Alzheimer’s Disease (JPAD). http://dx.doi.org/10.14283/jpad.2016.115

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‘ALZHEIMER’S PROGRESSION SCORE’: DEVELOPMENT OF A BIOMARKER SUMMARY OUTCOME FOR AD PREVENTION TRIALS

J.-M. Leoutsakos, A.L. Gross, R.N. Jones, M.S. Albert, J.C.S. Breitner

J Prev Alz Dis 2016;3(4):229-235

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Background: Alzheimer’s disease (AD) prevention research requires methods for measurement of disease progression not yet revealed by symptoms. Preferably, such measurement should encompass multiple disease markers. Objectives: Evaluate an item response theory (IRT) model-based latent variable Alzheimer Progression Score (APS) that uses multi-modal disease markers to estimate pre-clinical disease progression. Design: Estimate APS scores in the BIOCARD observational study, and in the parallel PREVENT-AD Cohort and its sister INTREPAD placebo-controlled prevention trial. Use BIOCARD data to evaluate whether baseline and early APS trajectory predict later progression to MCI/dementia. Similarly, use longitudinal PREVENT-AD data to assess test measurement invariance over time. Further, assess portability of the PREVENT-AD IRT model to baseline INTREPAD data, and explore model changes when CSF markers are added or withdrawn. Setting: BIOCARD was established in 1995 and participants were followed up to 20 years in Baltimore, USA. The PREVENT-AD and INTREPAD trial cohorts were established between 2011-2015 in Montreal, Canada, using nearly identical entry criteria to enroll high-risk cognitively normal persons aged 60+ then followed for several years. Participants: 349 cognitively normal, primarily middle-aged participants in BIOCARD, 125 high-risk participants aged 60+ in PREVENT-AD, and 217 similar subjects in INTREPAD. 106 INTREPAD participants donated up to four serial CSF samples. Measurements: Global cognitive assessment and multiple structural, functional, and diffusion MRI metrics, sensori-neural tests, and CSF concentrations of tau, Aβ42 and their ratio. Results: Both baseline values and early slope of APS scores in BIOCARD predicted later progression to MCI or AD. Presence of CSF variables strongly improved such prediction. A similarly derived APS in PREVENT-AD showed measurement invariance over time and portability to the parallel INTREPAD sample. Conclusions: An IRT-based APS can summarize multi-modal information to provide a longitudinal measure of pre-clinical AD progression, and holds promise as an outcome for AD prevention trials.

CITATION:
J.-M. Leoutsakos ; A.L. Gross ; R.N. Jones ; M.S. Albert ; J.C.S. Breitner (2016): ‘Alzheimer’s Progression Score’: Development of a Biomarker Summary Outcome for AD Prevention Trials. The Journal of Prevention of Alzheimer’s Disease (JPAD). http://dx.doi.org/10.14283/jpad.2016.120

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Contemporary Issues

RATIONALE AND STRUCTURE FOR A NEW CENTER FOR STUDIES ON PREVENTION OF ALZHEIMER’S DISEASE (STOP-AD)

J.C.S. Breitner, J. Poirier, P.E. Etienne, J.M. Leoutsakos, for the PREVENT-AD Research Group

J Prev Alz Dis 2016;3(4):236-242

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We describe events spanning over 20 years that have shaped our approach to identification of interventions that may delay symptoms in Alzheimer’s disease (AD). These events motivated the development of a new Centre for Studies on Prevention of AD that includes an observational cohort of cognitively normal high-risk persons and INTREPAD, a nested two-year randomized placebo-controlled trial of the non-steroidal anti-inflammatory drug naproxen sodium. INTREPAD enrolled 217 persons and will follow 160 in a modified intent-to-treat analysis of persons who remained on-protocol through at least one follow-up evaluation. The trial employs dual endpoints: 1) a composite global cognitive score generated by a battery of 12 psychometric tests organized into five subscales; and 2) a summary Alzheimer’s Progression Score derived from latent variable modeling of multiple biomarker data from several modalities. The dual endpoints will be analyzed by consideration of their joint probability under the null hypothesis of no treatment effect, after allowing appropriately for their lack of independence. We suggest that such an approach can be used economically to generate preliminary data regarding the efficacy of potential prevention strategies, thereby increasing the chances of finding one or more interventions that successfully prevent symptoms.

CITATION:
J.C.S. Breitner ; J. Poirier ; P.E. Etienne ; J.M. Leoutsakos for the PREVENT-AD Research Group (2016): Rationale and Structure for a New Center for Studies on Prevention of Alzheimer’s Disease (StoP-AD). The Journal of Prevention of Alzheimer’s Disease (JPAD). http://dx.doi.org/10.14283/jpad.2016.121

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Review Articles

PRECISION MEDICINE - THE GOLDEN GATE FOR DETECTION, TREATMENT AND PREVENTION OF ALZHEIMER’S DISEASE

H. Hampel, S.E. O’Bryant, J.I. Castrillo, C. Ritchie, K. Rojkova, K. Broich, N. Benda, R. Nisticò, R.A. Frank, B. Dubois, V. Escott-Price, S. Lista

J Prev Alz Dis 2016;3(4):243-259

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During this decade, breakthrough conceptual shifts have commenced to emerge in the field of Alzheimer’s disease (AD) recognizing risk factors and the non-linear dynamic continuum of complex pathophysiologies amongst a wide dimensional spectrum of multi-factorial brain proteinopathies/neurodegenerative diseases. As is the case in most fields of medicine, substantial advancements in detecting, treating and preventing AD will likely evolve from the generation and implementation of a systematic precision medicine strategy. This approach will likely be based on the success found from more advanced research fields, such as oncology. Precision medicine will require integration and transfertilization across fragmented specialities of medicine and direct reintegration of Neuroscience, Neurology and Psychiatry into a continuum of medical sciences away from the silo approach. Precision medicine is biomarker-guided medicine on systems-levels that takes into account methodological advancements and discoveries of the comprehensive pathophysiological profiles of complex multi-factorial neurodegenerative diseases, such as late-onset sporadic AD. This will allow identifying and characterizing the disease processes at the asymptomatic preclinical stage, where pathophysiological and topographical abnormalities precede overt clinical symptoms by many years to decades. In this respect, the uncharted territory of the AD preclinical stage has become a major research challenge as the field postulates that early biomarker guided customized interventions may offer the best chance of therapeutic success. Clarification and practical operationalization is needed for comprehensive dissection and classification of interacting and converging disease mechanisms, description of genomic and epigenetic drivers, natural history trajectories through space and time, surrogate biomarkers and indicators of risk and progression, as well as considerations about the regulatory, ethical, political and societal consequences of early detection at asymptomatic stages. In this scenario, the integrated roles of genome sequencing, investigations of comprehensive fluid-based biomarkers and multimodal neuroimaging will be of key importance for the identification of distinct molecular mechanisms and signaling pathways in subsets of asymptomatic people at greatest risk for progression to clinical milestones due to those specific pathways. The precision medicine strategy facilitates a paradigm shift in Neuroscience and AD research and development away from the classical “one-size-fits-all” approach in drug discovery towards biomarker guided “molecularly” tailored therapy for truly effective treatment and prevention options. After the long and winding decade of failed therapy trials progress towards the holistic systems-based strategy of precision medicine may finally turn into the new age of scientific and medical success curbing the global AD epidemic.

CITATION:
H. Hampel ; S.E. O’Bryant ; J.I. Castrillo ; C. Ritchie ; K. Rojkova ; K. Broich ; N. Benda ; R. Nisticò ; R.A. Frank ; B. Dubois ; V. Escott-Price ; S. Lista (2016): PRECISION MEDICINE - The Golden Gate for Detection, Treatment and Prevention of Alzheimer’s Disease. The Journal of Prevention of Alzheimer’s Disease (JPAD). http://dx.doi.org/10.14283/jpad.2016.112

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Clinical Trials and Aging: 9th Conference Clinical Trials on Alzheimer’s Disease, December 8-10, 2016, San Diego, USA

CTAD: SYMPOSIA, ORAL COMMUNICATIONS, POSTERS

Abstracts

J Prev Alz Dis 2016;4:262-379

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