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Table representation of search results timeline featuring number of search results per year.

Year Number of Results
1984 2
1985 2
1986 3
1987 24
1988 44
1989 82
1990 101
1991 169
1992 163
1993 204
1994 263
1995 293
1996 348
1997 390
1998 403
1999 431
2000 560
2001 619
2002 789
2003 817
2004 904
2005 1026
2006 1109
2007 1148
2008 1349
2009 1608
2010 1769
2011 1777
2012 1983
2013 2068
2014 2116
2015 2221
2016 2248
2017 2277
2018 2336
2019 1008
2020 17
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29,262 results
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Page 1
Platelet-generated amyloid beta peptides in Alzheimer's disease and glaucoma.
Inyushin M, et al. Histol Histopathol 2019 - Review. PMID 30945258 Free PMC article.
Amyloid beta (Aβ) peptides have been implicated in both Alzheimer's disease (AD) and glaucoma and have been shown to be the key etiological factor in these dangerous health complications. ...The correlation between the effect on platelet count and the effectiveness of anti-AD and anti-glaucoma therapies suggest that platelets may be an important player in these diseases....
Amyloid beta (Aβ) peptides have been implicated in both Alzheimer's disease (AD) and glaucoma and have been show
Amyloid Beta and Phosphorylated Tau-Induced Defective Autophagy and Mitophagy in Alzheimer's Disease.
Reddy PH and Oliver DM. Cells 2019 - Review. PMID 31121890 Free PMC article.
Several decades of intense research have revealed that multiple cellular changes are implicated in the development and progression of AD, including mitochondrial damage, synaptic dysfunction, amyloid beta (Aβ) formation and accumulation, hyperphosphorylated tau (P-Tau) formation and accumulation, deregulated microRNAs, synaptic damage, and neuronal loss in patients with AD. ...In addition, abnormal interactions between (1) Aβ and mitochondrial fission protein Drp1; (2) P-Tau and Drp1; and (3) Aβ and PINK1/parkin lead to an inability to clear damaged mitochondria and other cellular debris from neurons. ...
Several decades of intense research have revealed that multiple cellular changes are implicated in the development and progression of AD, in …
Genetic meta-analysis of diagnosed Alzheimer's disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing
Kunkle BW, et al. Nat Genet 2019. Among authors: Becker JT, Bennett D, Beecham GW, Bellenguez C, Benito YA, Ben-Shlomo Y, Beekly D, Beach TG, Berr C, Beiser AS. PMID 30820047 Free PMC article.
Analyses of risk genes and pathways show enrichment for rare variants (P = 1.32 × 10(-7)), indicating that additional rare variants remain to be identified. We also identify important genetic correlations between LOAD and traits such as family history of dementia and education....
Analyses of risk genes and pathways show enrichment for rare variants (P = 1.32 × 10(-7)), indicating that additional rare variants remain t …
Ketogenic Diet in Alzheimer's Disease
Rusek M, et al. Int J Mol Sci 2019 - Review. PMID 31405021 Free PMC article.
Although the mechanism of the underlying pathology is not fully uncovered, in the last years, there has been significant progress in its understanding. This includes: Progressive deposition of amyloid β-peptides in amyloid plaques and hyperphosphorylated tau protein in intracellular as neurofibrillary tangles; neuronal loss; and impaired glucose metabolism. ...
Although the mechanism of the underlying pathology is not fully uncovered, in the last years, there has been significant progress in …
Multi-sensory Gamma Stimulation Ameliorates Alzheimer's-Associated Pathology and Improves Cognition
Martorell AJ, et al. Cell 2019. PMID 30879788 Free PMC article.
Seven days of auditory GENUS improved spatial and recognition memory and reduced amyloid in AC and hippocampus of 5XFAD mice. ...Thus, GENUS can be achieved through multiple sensory modalities with wide-ranging effects across multiple brain areas to improve cognitive function....
Seven days of auditory GENUS improved spatial and recognition memory and reduced amyloid in AC and hippocampus of 5XFAD mice. ...Thus …
Randomized Trial of Verubecestat for Prodromal Alzheimer's Disease
Egan MF, et al. N Engl J Med 2019 - Clinical Trial. PMID 30970186 Free PMC article.
BACKGROUND: Prodromal Alzheimer's disease offers an opportunity to test the effect of drugs that modify the deposition of amyloid in the brain before the onset of dementia. Verubecestat is an orally administered β-site amyloid precursor protein-cleaving enzyme 1 (BACE-1) inhibitor that blocks production of amyloid-beta (Aβ). ...
BACKGROUND: Prodromal Alzheimer's disease offers an opportunity to test the effect of drugs that modify the deposition of amyloid in …
Senolytic therapy alleviates Aβ-associated oligodendrocyte progenitor cell senescence and cognitive deficits in an Alzheimer's disease model
Zhang P, et al. Nat Neurosci 2019. PMID 30936558 Free PMC article.
Neuritic plaques, a pathological hallmark in Alzheimer's disease (AD) brains, comprise extracellular aggregates of amyloid-beta (Aβ) peptide and degenerating neurites that accumulate autolysosomes. ...Our findings suggest a role for Aβ-induced OPC cell senescence in neuroinflammation and cognitive deficits in AD, and a potential therapeutic benefit of senolytic treatments....
Neuritic plaques, a pathological hallmark in Alzheimer's disease (AD) brains, comprise extracellular aggregates of amyloid-beta
Nanomedicine in Alzheimer's disease: Amyloid beta targeting strategy.
Tosi G, et al. Prog Brain Res 2019 - Review. Among authors: Belletti D. PMID 30961872
The reasons could be ascribed on two main factors: (i) lack of ability of the majority of drugs to cross the blood-brain barrier (BBB), thus excluding the brain for any successful therapy; (ii) lack of selectivity and specificity of drugs, decreasing the efficacy of even potent anti-AD drugs. The exploitation of specifically engineered nanomedicines planned to cross the BBB and to target the most "hot" site of action (i.e., β-amyloid) is one of the most interesting innovations in drug delivery and could reasonably represent an promising choice for possible treatments and even early-diagnosis of AD. ...
The reasons could be ascribed on two main factors: (i) lack of ability of the majority of drugs to cross the blood-brain barrier (BBB …
Contributions of Mass Spectrometry to the Identification of Low Molecular Weight Molecules Able to Reduce the Toxicity of Amyloid-β Peptide to Cell Cultures and Transgenic Mouse Models of Alzheimer's Disease.
Ştefănescu R, et al. Molecules 2019 - Review. PMID 30909659 Free PMC article.
The formation of toxic amyloid oligomers, extracellular amyloid plaques and amyloid angiopathy in brain by amyloid beta peptides are considered a part of the identified mechanism involved in disease pathogenesis. ...In the present review we aim to identify in the scientific literature low molecular weight chemical compounds for which there is mass spectrometric evidence of noncovalent complex formation with amyloid peptides and also there are toxicity reduction results which verify the effects of these compounds on amyloid beta toxicity towards cell cultures and transgenic mouse models developing Alzheimer's Disease....
The formation of toxic amyloid oligomers, extracellular amyloid plaques and amyloid angiopathy in brain by amyloid
Alzheimer's disease: pathogenesis, diagnostics, and therapeutics
Tiwari S, et al. Int J Nanomedicine 2019 - Review. PMID 31410002 Free PMC article.
AD is a neurodegenerative disease, and its pathogenesis has been attributed to extracellular aggregates of amyloid β (Aβ) plaques and intracellular neurofibrillary tangles made of hyperphosphorylated τ-protein in cortical and limbic areas of the human brain. ...In addition to a detailed report on causative factors leading to AD, the present review also discusses the current state of the art in AD therapeutics and diagnostics, including labeling and imaging techniques employed as contrast agents for better visualization and sensing of the plaques. ...
AD is a neurodegenerative disease, and its pathogenesis has been attributed to extracellular aggregates of amyloid β (Aβ) plaq …
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