Amyloid β oligomers in Alzheimer's disease pathogenesis, treatment, and diagnosis

KL Viola, WL Klein - Acta neuropathologica, 2015 - Springer
Protein aggregation is common to dozens of diseases including prionoses, diabetes,
Parkinson's and Alzheimer's. Over the past 15 years, there has been a paradigm shift in …

[HTML][HTML] Soluble amyloid-β oligomers as synaptotoxins leading to cognitive impairment in Alzheimer's disease

ST Ferreira, MV Lourenco, MM Oliveira… - Frontiers in cellular …, 2015 - frontiersin.org
Alzheimer's disease (AD) is the most common form of dementia in the elderly, and affects
millions of people worldwide. As the number of AD cases continues to increase in both …

C-terminally truncated forms of tau, but not full-length tau or its C-terminal fragments, are released from neurons independently of cell death

D Kanmert, A Cantlon, CR Muratore, M Jin… - Journal of …, 2015 - Soc Neuroscience
Recent evidence suggests that tau aggregation may spread via extracellular release and
subsequent uptake by synaptically connected neurons, but little is known about the …

Possible role of resveratrol targeting estradiol and neprilysin pathways in lipopolysaccharide model of Alzheimer disease

NS El-Sayed, Y Bayan - GeNeDis 2014: Neurodegeneration, 2015 - Springer
Alzheimer's disease (AD) is an irreversible, progressive neurodegenerative brain disease
that slowly destroys memory and thinking skills. It is the most common cause of dementia …

Calcium channel blockers, progression to dementia, and effects on amyloid beta peptide production

MA Lovell, E Abner, R Kryscio, L Xu… - Oxidative medicine …, 2015 - Wiley Online Library
Previous epidemiologic studies suggest that antihypertensive drugs may be protective
against cognitive decline. To determine if subjects enrolled in the University of Kentucky …

[HTML][HTML] Acute intracerebral treatment with amyloid-beta (1–42) alters the profile of neuronal oscillations that accompany LTP induction and results in impaired LTP in …

AN Kalweit, H Yang, J Colitti-Klausnitzer… - Frontiers in behavioral …, 2015 - frontiersin.org
Accumulation of amyloid plaques comprises one of the major hallmarks of Alzheimer's
disease (AD). In rodents, acute treatment with amyloid-beta (Aβ; 1–42) elicits immediate …

[HTML][HTML] Amyloid β oligomeric species present in the lag phase of amyloid formation

M Wolff, D Unuchek, B Zhang, V Gordeliy, D Willbold… - PloS one, 2015 - journals.plos.org
Alzheimer's disease (AD)-associated amyloid β peptide (Aβ) is one of the main actors in AD
pathogenesis. Aβ is characterized by its high tendency to self-associate, leading to the …

NGF but not BDNF overexpression protects hippocampal LTP from beta-amyloid-induced impairment

AD Ivanov, GR Tukhbatova, SV Salozhin… - Neuroscience, 2015 - Elsevier
Two major neurotrophic factors, nerve growth factor (NGF) and brain-derived neurotrophic
factor (BDNF) are involved in a number of physiological processes associated with neuronal …

Cellular and network mechanisms underlying memory impairment induced by amyloid β protein

K Salgado-Puga, F Pena-Ortega - Protein and peptide letters, 2015 - ingentaconnect.com
It has long been known that amyloid ß protein (Aß) plays a key role in Alzheimer's Disease
(AD) and in Down Syndrome cognitive decline. Recent findings have shown that soluble …

Lentiviral-mediated overexpression of nerve growth factor (NGF) prevents beta-amyloid [25–35]-induced long term potentiation (LTP) decline in the rat hippocampus

SS Uzakov, AD Ivanov, SV Salozhin, VA Markevich… - Brain research, 2015 - Elsevier
We have explored the potential neuroprotective effect of local lentiviraly-mediated
overexpression of nerve growth factor (NGF) on in vivo long-term potentiation (LTP) in the rat …