Neurovascular dysfunction and vascular amyloid accumulation as early events in Alzheimer's disease

2021 ◽  
Author(s):  
Ricardo Apátiga-Pérez ◽  
Luis O. Soto-Rojas ◽  
B. Berenice Campa-Córdoba ◽  
Nabil Itzi Luna-Viramontes ◽  
Elvis Cuevas ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Accumulation ◽  
Neurovascular Dysfunction

Crossed Cerebellar Diaschisis in Alzheimer’s Disease

2018 ◽  
Vol 15 (13) ◽  
pp. 1267-1275 ◽  
Author(s):  
F.E. Reesink ◽  
D. Vállez García ◽  
C.A. Sánchez-Catasús ◽  
D.E. Peretti ◽  
A.T. Willemsen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Left Hemisphere ◽  
Pet Imaging ◽  
Fdg Pet ◽  
Pathophysiological Mechanism ◽  
Crossed Cerebellar Diaschisis ◽  
Amyloid Accumulation ◽  
Cerebellar Diaschisis ◽  
18F Fdg

Background: We describe the phenomenon of crossed cerebellar diaschisis (CCD) in four subjects diagnosed with Alzheimer’s disease (AD) according to the National Institute on Aging - Alzheimer Association (NIA-AA) criteria, in combination with 18F-FDG PET and 11C-PiB PET imaging. Methods: 18F-FDG PET showed a pattern of cerebral metabolism with relative decrease most prominent in the frontal-parietal cortex of the left hemisphere and crossed hypometabolism of the right cerebellum. 11C-PiB PET showed symmetrical amyloid accumulation, but a lower relative tracer delivery (a surrogate of relative cerebral blood flow) in the left hemisphere. CCD is the phenomenon of unilateral cerebellar hypometabolism as a remote effect of supratentorial dysfunction of the brain in the contralateral hemisphere. The mechanism implies the involvement of the cortico-ponto-cerebellar fibers. The pathophysiology is thought to have a functional or reversible basis but can also reflect in secondary morphologic change. CCD is a well-recognized phenomenon, since the development of new imaging techniques, although scarcely described in neurodegenerative dementias. Results: To our knowledge this is the first report describing CCD in AD subjects with documentation of both 18F-FDG PET and 11C-PiB PET imaging. CCD in our subjects was explained on a functional basis due to neurodegenerative pathology in the left hemisphere. There was no structural lesion and the symmetric amyloid accumulation did not correspond with the unilateral metabolic impairment. Conclusion: This suggests that CCD might be caused by non-amyloid neurodegeneration. The pathophysiological mechanism, clinical relevance and therapeutic implications of CCD and the role of the cerebellum in AD need further investigation.

scholarly journals Brain amyloid accumulation and glucose hypometabolism in Chinese Alzheimer’s disease population

2020 ◽  
Vol 16 (S4) ◽  
Author(s):  
Shuhua Ren ◽  
Qi Huang ◽  
Donglang Jiang ◽  
Lin Huang ◽  
Ying Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Accumulation ◽  
Glucose Hypometabolism

scholarly journals Elevated Aβ and Apolipoprotein E in AβPP Transgenic Mice and Its Relationship to Amyloid Accumulation in Alzheimer’s Disease

2000 ◽  
Vol 6 (5) ◽  
pp. 430-439 ◽  
Author(s):  
Yu-Min Kuo ◽  
Fiona Crawford ◽  
Michael Mullan ◽  
Tyler A. Kokjohn ◽  
Mark R. Emmerling ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Apolipoprotein E ◽  
Amyloid Accumulation

scholarly journals Treatment with a Copper-Zinc Chelator Markedly and Rapidly Inhibits β-Amyloid Accumulation in Alzheimer's Disease Transgenic Mice

Neuron ◽  
2001 ◽  
Vol 30 (3) ◽  
pp. 665-676 ◽  
Author(s):  
Robert A Cherny ◽  
Craig S Atwood ◽  
Michel E Xilinas ◽  
Danielle N Gray ◽  
Walton D Jones ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Amyloid Accumulation ◽  
Zinc Chelator ◽  
Copper Zinc ◽  
Β Amyloid

scholarly journals Increased mtDNA mutations with aging promotes amyloid accumulation and brain atrophy in the APP/Ld transgenic mouse model of Alzheimer’s disease

2014 ◽  
Vol 9 (1) ◽  
pp. 16 ◽  
Author(s):  
Lokesh Kukreja ◽  
Gregory C Kujoth ◽  
Tomas A Prolla ◽  
Fred Van Leuven ◽  
Robert Vassar
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Brain Atrophy ◽  
Transgenic Mouse Model ◽  
Mtdna Mutations ◽  
Model Of Alzheimer’S Disease ◽  
Amyloid Accumulation

ASSOCIATION BETWEEN CEREBRAL AMYLOID ACCUMULATION AND SYNAPTIC DENSITY IN ALZHEIMER'S DISEASE: A MULTITRACER PET STUDY

2020 ◽  
Vol 28 (4) ◽  
pp. S123-S124
Author(s):  
Ryan O'Dell ◽  
Adam Mecca ◽  
Ming-Kai Chen ◽  
Tyler Godek ◽  
Joanna Harris ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Density ◽  
Amyloid Accumulation ◽  
Cerebral Amyloid

IC-P-156: Baseline amyloid PET imaging, longitudinal amyloid accumulation, and Tau PET imaging in preclinical Alzheimer's disease

2015 ◽  
Vol 11 (7S_Part_2) ◽  
pp. P105-P105
Author(s):  
Aaron P. Schultz ◽  
Elizabeth C. Mormino ◽  
Jasmeer P. Chhatwal ◽  
Molly LaPoint ◽  
Alex S. Dagley ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Pet Imaging ◽  
Amyloid Pet ◽  
Preclinical Alzheimer’S Disease ◽  
Amyloid Accumulation ◽  
Tau Pet ◽  
Tau Pet Imaging ◽  
Amyloid Pet Imaging

Features of molecule expression markers of insulin resistance in experimental Alzheimer’s disease

2015 ◽  
Vol 61 (4) ◽  
pp. 43-48
Author(s):  
Ya V Gorina ◽  
Yu K Komleva ◽  
O L Lopatina ◽  
V V Volkova ◽  
G E Gersog ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Alzheimer's Disease ◽  
Molecular Markers ◽  
Molecular Mechanisms ◽  
Cognitive Disorders ◽  
Brain Regions ◽  
Significant Loss ◽  
Amyloid Accumulation ◽  
The Central Nervous System

Alzheimer’s Disease (AD) is characterized by a significant loss of neurons and synapses, especially in the hippocampus and cortex, the extracellular β-amyloid accumulation and formation of neurofibrillary tangles. Insulin resistance plays important role in neurodegeneration and cognitive disorders in the central nervous system, especially AD. However, the cellular and molecular mechanisms that connect insulin resistance and Alzheimer’s pathogenesis remain largely unexplained. Therefore, great importance is the identification of molecular markers that allow to define new approaches to targeted pharmacological correction of neurodegeneration. This article describes the study of the expression of molecular markers, namely, IRAP, GLUT4, and IL-18 in different brain regions (hippocampus, olfactory bulb) rats with experimental AD

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