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Open AccessJournal ArticleDOI

Current and future treatments for Alzheimer's disease.

TLDR
Current symptomatic treatments and new potential disease-modifying therapies for AD that are currently being studied in phase I–III trials are discussed.
Abstract
Alzheimer’s dementia (AD) is increasingly being recognized as one of the most important medical and social problems in older people in industrialized and non-industrialized nations. To date, only symptomatic treatments exist for this disease, all trying to counterbalance the neurotransmitter disturbance. Three cholinesterase inhibitors (CIs) are currently available and have been approved for the treatment of mild to moderate AD. A further therapeutic option available for moderate to severe AD is memantine, an N-methyl-D-aspartate receptor noncompetitive antagonist. Treatments capable of stopping or at least effectively modifying the course of AD, referred to as ‘disease-modifying’ drugs, are still under extensive research. To block the progression of the disease they have to interfere with the pathogenic steps responsible for the clinical symptoms, including the deposition of extracellular amyloid β plaques and intracellular neurofibrillary tangle formation, inflammation, oxidative damage, iron deregulati...

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Journal ArticleDOI

Current and Future Treatments in Alzheimer Disease: An Update.

TL;DR: A review of disease-modifying therapies for Alzheimer disease can be found in this paper, where the authors discuss potential disease modifying therapies that are currently being studied and potential individualized therapeutic frameworks that can be proved beneficial for patients with AD.
Journal ArticleDOI

Design and synthesis of curcumin analogues for in vivo fluorescence imaging and inhibiting copper-induced cross-linking of amyloid beta species in Alzheimer's disease.

TL;DR: Curcumin-based near-infrared fluorescence imaging probes for detecting both soluble and insoluble amyloid beta (Aβ) species and then an inhibitor that could attenuate cross-linking of Aβ induced by copper are designed and synthesized.
Journal ArticleDOI

The multiplex model of the genetics of Alzheimer’s disease

TL;DR: The multiplex model reflects the combination of some, or all, of these model components (genetic and environmental), in a tissue-specific manner, to trigger or sustain a disease cascade, which ultimately results in the cell and synaptic loss observed in AD.
Journal ArticleDOI

Monoaminergic neuropathology in Alzheimer's disease.

TL;DR: Special emphasis is given to the serotonergic dorsal raphe nucleus (DRN) and noradrenergic LC, among the first to be affected by tau protein abnormalities in the course of sporadic AD, causing behavioral and cognitive symptoms of variable severity.
References
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Journal ArticleDOI

Preserved cognitive function after 12 months of treatment with rivastigmine in mild Alzheimer's disease in comparison with untreated AD and MCI patients.

TL;DR: A clear beneficial effect of rivastigmine was shown on cognitive function for patients with mild AD and plasma values of ChE inhibition were associated with attention.
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A 25-week, open-label trial investigating rivastigmine transdermal patches with concomitant memantine in mild-to-moderate Alzheimer's disease: a post hoc analysis.

TL;DR: Use of the rivastigmine transdermal patch in patients on established memantine appears to be well-tolerated, with only modest, non-significant increases in AEs compared with monotherapy, and did not seem to affect cognition or global functioning adversely.
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Immunotherapy against APP beta-secretase cleavage site improves cognitive function and reduces neuroinflammation in Tg2576 mice without a significant effect on brain abeta levels.

TL;DR: Long-term systemic administration of anti-APP β-site antibodies to Tg2576 transgenic mice improved mouse cognitive functions associated with a reduction in both brain inflammation and the incidence of microhemorrhage, and antibody treatment did not induce any peripheral autoimmunity responses.
Journal ArticleDOI

Pharmacologists and Alzheimer disease therapy: to boldly go where no scientist has gone before

TL;DR: The discovery of new drugs efficacious in AD subjects is an ambitious goal, however, and one that will require close, active collaboration by pharmacologists, chemists and clinicians.
Journal ArticleDOI

Clinical observations with AN-1792 using TAPIR analyses.

TL;DR: Clinical observations with AN-1792 using tissue amyloid plaque immunoreactivity (TAPIR) analyses established for the first time evidence in humans that antibodies against β-amyloid-related epitopes are capable of slowing progression in Alzheimer’s disease.
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