Neuroprotective effect of 1-Deoxynojirimycin on cognitive impairment, β-amyloid deposition, and neuroinflammation in the SAMP8 mice

2018 ◽  
Vol 106 ◽  
pp. 92-97 ◽  
Author(s):  
Weike Chen ◽  
Tingting Liang ◽  
Wenwen Zuo ◽  
Xin Wu ◽  
Zibo Shen ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Neuroprotective Effect ◽  
Amyloid Deposition ◽  
Β Amyloid ◽  
Samp8 Mice

scholarly journals Rapid β-Amyloid Deposition and Cognitive Impairment After Cholinergic Denervation in APP/PS1 Mice

2013 ◽  
Vol 72 (4) ◽  
pp. 272-285 ◽  
Author(s):  
Juan Jose Ramos-Rodriguez ◽  
Mar Pacheco-Herrero ◽  
Diana Thyssen ◽  
Maria Isabel Murillo-Carretero ◽  
Esther Berrocoso ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Amyloid Deposition ◽  
Β Amyloid

P2-431: RELATIONSHIP BETWEEN LOCAL RESTING STATE ACTIVITY, β-AMYLOID DEPOSITION AND MEMORY PERFORMANCE IN THE DZNE: LONGITUDINAL COGNITIVE IMPAIRMENT AND DEMENTIA STUDY (DELCODE)

2006 ◽  
Vol 14 (7S_Part_16) ◽  
pp. P877-P878
Author(s):  
Coraline D. Metzger ◽  
Martin Dyrba ◽  
Daniel Bittner ◽  
Xiaochen Hu ◽  
Frank Jessen ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Resting State ◽  
Memory Performance ◽  
Amyloid Deposition ◽  
State Activity ◽  
Β Amyloid

scholarly journals Elevated occipital β-amyloid deposition is associated with widespread cognitive impairment in logopenic progressive aphasia

2013 ◽  
Vol 84 (12) ◽  
pp. 1357-1364 ◽  
Author(s):  
Jennifer L Whitwell ◽  
Val J Lowe ◽  
Joseph R Duffy ◽  
Edythe A Strand ◽  
Mary M Machulda ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Amyloid Deposition ◽  
Progressive Aphasia ◽  
Β Amyloid

P1-397: Sleep Disordered Breathing, CSF P-TAU, Hippocampal Atrophy and β-Amyloid Deposition in Mild Cognitive Impairment Patients

2016 ◽  
Vol 12 ◽  
pp. P585-P586
Author(s):  
Omonigho Michael Bubu ◽  
James Mortimer ◽  
David Morgan ◽  
Skai Schwartz ◽  
Amy Borenstein ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Sleep Disordered Breathing ◽  
Amyloid Deposition ◽  
Hippocampal Atrophy ◽  
Β Amyloid ◽  
Disordered Breathing

scholarly journals Spatial relationships between white matter degeneration, amyloid load and cortical volume in amnestic mild cognitive impairment

2018 ◽  
Author(s):  
Ileana O Jelescu ◽  
Timothy M Shepherd ◽  
Dmitry S Novikov ◽  
Yu-Shin Ding ◽  
Benjamin Ades-Aron ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
White Matter ◽  
Diffusion Mri ◽  
Amnestic Mild Cognitive Impairment ◽  
Amyloid Deposition ◽  
Cortical Volume ◽  
Cortical Areas ◽  
Healthy Control ◽  
Β Amyloid

The spatial-temporal relationships between gray and white matter (WM) degeneration during preclinical and early symptomatic Alzheimer's disease are poorly understood. We characterized β-amyloid deposition, cortical volume and WM degeneration in 44 subjects including healthy control (N=23), amnestic mild cognitive impairment (aMCI) (N=19), and early Alzheimer's subjects (N=2). Integrated PET-MRI provided simultaneous measurement of 18F-Florbetapir uptake in cortical areas, regional brain volumes from structural MRI, and WM tract integrity metrics from diffusion MRI using biophysical modeling. Across the cohort of healthy control and aMCIs, cortical volumes correlated poorly with β-amyloid deposition in the same area (p < 0.05 only in the posterior cingulate and parietal lobe). WM degeneration correlated significantly with both amyloid and volume of connected cortical areas, but more strongly with volume. Diffusion MRI metrics for WM demyelination and/or axonal loss could therefore provide new biomarkers associated with clinical Alzheimer's conversion. These WM changes may represent sequential propagation of Alzheimer's neurodegeneration between functionally connected regions, and/or evidence of direct WM injury during the Alzheimer's pathology cascade.

Metformin and Cyanidin 3-O-galactoside from Aronia melanocarpa Synergistically Alleviate Cognitive Impairment in SAMP8 mice

2021 ◽  
Author(s):  
Haichao Wen ◽  
Hehe Tian ◽  
Chang Liu ◽  
Xiaoxu Zhang ◽  
Xinquan Yang ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Neurodegenerative Disease ◽  
Neuroprotective Effect ◽  
Aronia Melanocarpa ◽  
Samp8 Mice

Cyanidin 3-O-galactoside (Cy3Gal) from Aronia melanocarpa has been reported in alleviating cognitive impairment. Metformin for preventing the neurodegenerative disease is causing increasing concern. However, both of them on neuroprotective effect...

Alzheimer’s Disease: Erythrocyte 2,3-diphosphoglycerate Content and Circulating Erythropoietin

2019 ◽  
Vol 16 (9) ◽  
pp. 834-835
Author(s):  
Petter Järemo ◽  
Alenka Jejcic ◽  
Vesna Jelic ◽  
Tasmin Shahnaz ◽  
Homira Behbahani ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Cell Damage ◽  
Control Group ◽  
Red Cell ◽  
Oxygen Release ◽  
Regulatory Pathways ◽  
Β Amyloid ◽  
2,3 Dpg

Background: Alzheimer’s Disease (AD) features the accumulation of β-amyloid in erythrocytes. The subsequent red cell damage may well affect their oxygen-carrying capabilities. 2,3- diphosphoglycerate (2,3-DPG) binds to the hemoglobin thereby promoting oxygen release. It is theorized that 2,3-DPG is reduced in AD and that the resulting hypoxia triggers erythropoietin (EPO) release. Methods & Objective: To explore this theory, we analyzed red cell 2,3-DPG content and EPO in AD, mild cognitive impairment, and the control group, subjective cognitive impairment. Results: We studied (i) 2,3-DPG in red cells, and (ii) circulating EPO in AD, and both markers were unaffected by dementia. Disturbances of these oxygen-regulatory pathways do not appear to participate in brain hypoxia in AD.

Biological Signatures of Alzheimer’s Disease

2020 ◽  
Vol 20 (9) ◽  
pp. 770-781 ◽  
Author(s):  
Poornima Sharma ◽  
Anjali Sharma ◽  
Faizana Fayaz ◽  
Sharad Wakode ◽  
Faheem H. Pottoo
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Senile Plaque ◽  
Senile Plaques ◽  
Amyloid Deposition ◽  
Immune Defense ◽  
Amyloid Angiopathy ◽  
Microvascular Changes ◽  
Β Amyloid

Alzheimer’s disease (AD) is the most prevalent and severe neurodegenerative disease affecting more than 0.024 billion people globally, more common in women as compared to men. Senile plaques and amyloid deposition are among the main causes of AD. Amyloid deposition is considered as a central event which induces the link between the production of β amyloid and vascular changes. Presence of numerous biomarkers such as cerebral amyloid angiopathy, microvascular changes, senile plaques, changes in white matter, granulovascular degeneration specifies the manifestation of AD while an aggregation of tau protein is considered as a primary marker of AD. Likewise, microvascular changes, activation of microglia (immune defense system of CNS), amyloid-beta aggregation, senile plaque and many more biomarkers are nearly found in all Alzheimer’s patients. It was seen that 70% of Alzheimer’s cases occur due to genetic factors. It has been reported in various studies that apolipoprotein E(APOE) mainly APOE4 is one of the major risk factors for the later onset of AD. Several pathological changes also occur in the white matter which include dilation of the perivascular space, loss of axons, reactive astrocytosis, oligodendrocytes and failure to drain interstitial fluid. In this review, we aim to highlight the various biological signatures associated with the AD which may further help in discovering multitargeting drug therapy.

scholarly journals Long-Term Caloric Restriction Attenuates β-Amyloid Neuropathology and Is Accompanied by Autophagy in APPswe/PS1delta9 Mice

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 985
Author(s):  
Luisa Müller ◽  
Nicole Power Guerra ◽  
Jan Stenzel ◽  
Claire Rühlmann ◽  
Tobias Lindner ◽  
...  
Keyword(s):  
Caloric Restriction ◽  
Neuroprotective Effect ◽  
Resonance Spectroscopy ◽  
Neuroprotective Effects ◽  
Beneficial Effects ◽  
Positron Emission ◽  
Pet Ct ◽  
Amyloid Aβ ◽  
Β Amyloid

Caloric restriction (CR) slows the aging process, extends lifespan, and exerts neuroprotective effects. It is widely accepted that CR attenuates β-amyloid (Aβ) neuropathology in models of Alzheimer’s disease (AD) by so-far unknown mechanisms. One promising process induced by CR is autophagy, which is known to degrade aggregated proteins such as amyloids. In addition, autophagy positively regulates glucose uptake and may improve cerebral hypometabolism—a hallmark of AD—and, consequently, neural activity. To evaluate this hypothesis, APPswe/PS1delta9 (tg) mice and their littermates (wild-type, wt) underwent CR for either 16 or 68 weeks. Whereas short-term CR for 16 weeks revealed no noteworthy changes of AD phenotype in tg mice, long-term CR for 68 weeks showed beneficial effects. Thus, cerebral glucose metabolism and neuronal integrity were markedly increased upon 68 weeks CR in tg mice, indicated by an elevated hippocampal fluorodeoxyglucose [18F] ([18F]FDG) uptake and increased N-acetylaspartate-to-creatine ratio using positron emission tomography/computer tomography (PET/CT) imaging and magnet resonance spectroscopy (MRS). Improved neuronal activity and integrity resulted in a better cognitive performance within the Morris Water Maze. Moreover, CR for 68 weeks caused a significant increase of LC3BII and p62 protein expression, showing enhanced autophagy. Additionally, a significant decrease of Aβ plaques in tg mice in the hippocampus was observed, accompanied by reduced microgliosis as indicated by significantly decreased numbers of iba1-positive cells. In summary, long-term CR revealed an overall neuroprotective effect in tg mice. Further, this study shows, for the first time, that CR-induced autophagy in tg mice accompanies the observed attenuation of Aβ pathology.

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