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July 02, 2014
Alzheimer's & Dementia: The Journal of the Alzheimer's Association May 2014
The MultiTEP platform–based Alzheimer's disease epitope
vaccine activates a broad repertoire of T helper cells in nonhuman primates
prelude to clinical trials we have characterized B- and T-cell immune responses
in macaques to AD vaccine candidates: AV-1955 and its slightly modified
version, AV-1959 (with 3 additional promiscuous Th epitopes).
Epitope-based DNA vaccine for Alzheimer's disease:
Translational study in macaques
trials with passive and active Alzheimer's disease (AD) vaccines suggest that
early interventions are needed for improvement of cognitive and/or functional
performance in patients, providing impetus for the development of safe and
immunologically potent active vaccines targeting amyloid β (Aβ). The AN-1792 trial
has indicated that Aβ-specific T cells may be unsafe for humans; therefore,
other vaccines based on small Aβ epitopes are undergoing preclinical and
Reduced 25-hydroxyvitamin D and
risk of Alzheimer’s disease and vascular dementia
D deficiency has been implicated as a risk factor for dementia in several
cross-sectional studies. We tested the hypothesis that reduced plasma
25-hydroxyvitamin D (25[OH]D) is associated with increased risk of Alzheimer’s
disease (AD) and vascular dementia in the general population.
Validity of dementia and
Alzheimer's disease diagnoses in Finnish national registers
investigated dementia and Alzheimer disease (AD) diagnoses in three national
registers in Finland: the Hospital Discharge Register (HDR), the Drug
Reimbursement Register, and the Causes of Death Register (CDR).
Australian population trends and
disparities in cholinesterase inhibitor use, 2003 to 2010
Australian Pharmaceutical Benefits Scheme (PBS) first subsidized cholinesterase
inhibitors (CEIs) for Alzheimer's disease in 2001, introducing a novel therapy
for a previously untreatable common condition. This study aims to determine
Australian rates of CEI use and to assess equality of access to treatment based
on socioeconomic status and geographic remoteness.
The source of cognitive
complaints predicts diagnostic conversion differentially among nondemented
objective of this study was to compare whether different sources of cognitive
complaint (i.e., subjective and informant) predict diagnostic conversion in
nondemented older adults.
Cognition and gait show a
distinct pattern of association in the general population
brain aging, cognition and gait deteriorate in several domains. However, the
interrelationship between cognitive and gait domains remains unclear. We
investigated the independent associations between cognitive and gait domains in
a community-dwelling population.
APOE interacts with age to modify rate of decline
in cognitive and brain changes in Alzheimer's disease
determine (1) whether age-standardized cognitive declines and brain
morphometric change differ between Young-Old patients with Alzheimer's disease
(YOAD) and Very-Old patients with Alzheimer's disease (VOAD), and (2) whether
the apolipoprotein E (APOE) genotype modifies these neuropsychological
and morphometric changes.
Effect of APOE genotype status on targeted
clinical trials outcomes and efficiency in dementia and mild cognitive
impairment resulting from Alzheimer's disease
apolipoprotein E (APOE) ε4 genotype has been recommended as a potential
inclusion or exclusion criterion in targeted clinical trials for Alzheimer's
disease (AD) and mild cognitive impairment (MCI) resulting from AD, and has
been implemented in trials of immunotherapeutic agents.
Parkinsonism and distinct
dementia patterns in a family with the MAPT R406W mutation
Arg406Trp (R406W) missense mutation in the microtubule-associated protein-tau
gene (MAPT) is a known cause of early-onset dementia. Various dementia
phenotypes have been described, including frontotemporal dementia (FTD), FTD
with parkinsonism, and early-onset Alzheimer disease (EOAD)-like presentations.
Variants in PPP3R1 and MAPT
are associated with more rapid functional decline in Alzheimer's disease: The
Cache County Dementia Progression Study
polymorphisms (SNPs) located in the gene encoding the regulatory subunit of the
protein phosphatase 2B (PPP3R1, rs1868402) and the
microtubule-associated protein tau (MAPT, rs3785883) gene were recently
associated with higher cerebrospinal fluid (CSF) tau levels in samples from the
Knight Alzheimer's Disease Research Center at Washington University (WU) and
Alzheimer's Disease Neuroimaging Initiative (ADNI). In these same samples, these
SNPs were also associated with faster functional decline, or progression of
Alzheimer's disease (AD) as measured by the Clinical Dementia Rating sum of
boxes scores (CDR-sb). We attempted to validate the latter association in an
independent, population-based sample of incident AD cases from the Cache County
Dementia Progression Study (DPS).
The amyloid hypothesis, time to
move on: Amyloid is the downstream result, not cause, of Alzheimer's disease
The “amyloid hypothesis” has
dominated Alzheimer research for more than 20 years, and proposes that
amyloid is the toxic cause of neural/synaptic damage and dementia. If correct,
decreasing the formation or removing amyloid should be therapeutic. Despite
discrepancies in the proposed mechanism, and failed clinical trials, amyloid
continues to be considered the cause of a degenerative cascade. Alternative
hypotheses must explain three features: (i) why amyloid toxicity is not
the etiology of Alzheimer's disease (AD), (ii) what alternative
mechanisms cause the degeneration and dementia of AD, and (iii) why
increased amyloid accumulates in the brain in AD. We propose that AD, which
occurs in elderly, already vulnerable brains, with multiple age-related
changes, is precipitated by impaired microvascular function, resulting
primarily from decreased Notch-related angiogenesis. With impaired
microvasculature, a lack of vascular endothelial-derived trophic factors and
decreased cerebral blood flow cause the atrophy of neural structures.
Therapeutic strategies should focus on supporting normal angiogenesis.
CSF Aβ1-42 combined with
neuroimaging biomarkers in the early detection, diagnosis and prediction of
The development of validated,
qualified, and standardized biomarkers for Alzheimer's disease (AD) that allow
for an early presymptomatic diagnosis and discrimination (classification) from
other types of dementia and neurodegenerative diseases is warranted to
accelerate the successful development of novel disease-modifying therapies.
Mitochondrial DNA deletions in
Alzheimer's brains: A review
Mitochondrial dysfunction and
increased oxidative stress have been associated with normal aging and are
possibly implicated in the etiology of late-onset Alzheimer's disease (AD). DNA
deletions, as well as other alterations, can result from oxidative damage to
nucleic acids. Many studies during the past two decades have investigated the
incidence of mitochondrial DNA deletions in postmortem brain tissues of
late-onset AD patients compared with age-matched normal control subjects.
Published studies are not entirely concordant, but their differences might shed
light on the heterogeneity of AD itself. Our understanding of the role that
mitochondrial DNA deletions play in disease progression may provide valuable
information that could someday lead to a treatment.
The ε4 genotype of
apolipoprotein E and white matter integrity in Alzheimer's disease
multicenter study, we investigated a possible association between the APOE
ε4 allele and white matter (WM) integrity in Alzheimer's disease (AD) using
diffusion tensor imaging (DTI).
Disease Research Portfolio (IADRP) aims to capture global Alzheimer's disease
The goal of the IADRP project
is to enable funding organizations to assess the changing landscape of AD
research and coordinate strategies, leverage resources, and avoid duplication
Design of a comprehensive
Alzheimer’s disease clinic and research center in Spain to meet critical
patient and family needs
disease (AD) affects people worldwide, and the prevalence is increasing as the
population ages. There is an international effort to understand the biology of
AD to develop primary and secondary prevention strategies, and to develop
effective therapeutic interventions for individuals who are already
symptomatic. One of the critically important pieces of all national plans to
address AD is the call for the development of service models to deliver
quality, effective care based on the best evidence available.