scholarly journals Stable Size Distribution of Amyloid Plaques Over the Course of Alzheimer Disease

2012 ◽  
Vol 71 (8) ◽  
pp. 694-701 ◽  
Author(s):  
Alberto Serrano-Pozo ◽  
Matthew L. Mielke ◽  
Alona Muzitansky ◽  
Teresa Gómez-Isla ◽  
John H. Growdon ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Size Distribution ◽  
Amyloid Plaques ◽  
Stable Size Distribution

scholarly journals How early can we diagnose Alzheimer disease (and is it sufficient)?

Neurology ◽  
2018 ◽  
Vol 91 (9) ◽  
pp. 395-402 ◽  
Author(s):  
Ronald C. Petersen
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Alzheimer Disease ◽  
Clinical Symptoms ◽  
Amyloid Plaques ◽  
Clinical Syndrome ◽  
Cognitive Changes ◽  
Diagnostic Capability ◽  
Final Answer ◽  
Made In

A seismic shift in our understanding of the ability to diagnose Alzheimer disease (AD) is occurring. For the last several decades, AD has been a clinical–pathologic diagnosis, and this conceptualization of the disease has served the field well. Typically, the clinician would identify a syndrome such as mild cognitive impairment or dementia, and label the condition as “probable AD” since the diagnosis of definite AD could not be made until an autopsy revealed the presence of amyloid plaques and tau-based neurofibrillary tangles. However, with the advent of biomarkers for AD including neuroimaging and CSF, the identification of AD pathology can be made in life, which greatly enhances the ability of clinicians to be precise about the underlying etiology of a clinical syndrome. Hypothetical models of the temporal relation among the pathologic elements and the clinical symptoms have been proposed and have influenced the field enormously. This has enabled clinicians to be specific about the underlying cause of a given clinical syndrome. As such, the diagnostic capability of the clinician is evolving. However, AD pathology is only a component of the puzzle describing the causes of cognitive changes in aging. Most often, there is a multitude of pathologic entities contributing to the neuropathologic explanation of cognitive changes in aging. AD changes contribute important elements to the diagnosis, but the final answer is more complex. The field of aging and dementia will have to incorporate these additional elements.

Serial reconstruction of β-protein amyloid plaques: relationship to microvessels and size distribution

1992 ◽  
Vol 592 (1-2) ◽  
pp. 278-282 ◽  
Author(s):  
Mitsuru Kawai ◽  
Patrick Cras ◽  
George Perry
Keyword(s):  
Size Distribution ◽  
Amyloid Plaques ◽  
Β Protein

scholarly journals A numerical study on the estimation of the stable size distribution for a cell population balance model

2018 ◽  
Vol 41 (8) ◽  
pp. 2894-2905 ◽  
Author(s):  
Luis M. Abia ◽  
Óscar Angulo ◽  
Juan Carlos López-Marcos ◽  
Miguel Ángel López-Marcos
Keyword(s):  
Size Distribution ◽  
Cell Population ◽  
Numerical Study ◽  
Population Balance ◽  
Balance Model ◽  
Population Balance Model ◽  
A Cell ◽  
Stable Size Distribution

Loss of Lysosomal Proteins Progranulin and Prosaposin Associated with Increased Neurofibrillary Tangle Development in Alzheimer Disease

2021 ◽  
Author(s):  
Anarmaa Mendsaikhan ◽  
Ikuo Tooyama ◽  
Geidy E Serrano ◽  
Thomas G Beach ◽  
Douglas G Walker
Keyword(s):  
Alzheimer Disease ◽  
Human Brain ◽  
Tau Protein ◽  
Neurofibrillary Tangle ◽  
Neuronal Loss ◽  
Amyloid Plaques ◽  
Human Brain Tissue ◽  
Tissue Sections ◽  
Disease Modifying ◽  
Lysosomal Proteins

Abstract Alzheimer disease (AD) is a progressive neurodegenerative disease causing cognitive decline in the aging population. To develop disease-modifying treatments, understanding the mechanisms behind the pathology is important, which should include observations using human brain samples. We reported previously on the association of lysosomal proteins progranulin (PGRN) and prosaposin (PSAP) with amyloid plaques in non-demented aged control and AD brains. In this study, we investigated the possible involvement of PGRN and PSAP in tangle formation using human brain tissue sections of non-demented aged control subjects and AD cases and compared with cases of frontotemporal dementia with granulin (GRN) mutations. The study revealed that decreased amounts of PGRN and PSAP proteins were detected even in immature neurofibrillary tangles, while colocalization was still evident in adjacent neurons in all cases. Results suggest that neuronal loss of PGRN preceded loss of PSAP as tangles developed and matured. The GRN mutation cases exhibited almost complete absence of PGRN in most neurons, while PSAP signal was preserved. Although based on correlative data, we suggest that reduced levels of PGRN and PSAP and their interaction in neurons might predispose to accumulation of p-Tau protein.

STABLE SIZE DISTRIBUTION IN A MATHEMATICAL MODEL FOR TUMOR CELL POPULATION GROWTH DURING CHEMOTHERAPEUTICAL TREATMENT WITH TWO NON-CROSS RESISTANT DRUGS

1999 ◽  
Vol 07 (03) ◽  
pp. 285-306
Author(s):  
HAMILTON F. LECKAR ◽  
LAÉRCIO L. VENDITE
Keyword(s):  
Tumor Cell ◽  
Size Distribution ◽  
Genetic Mutation ◽  
Mixed Population ◽  
Linear Partial Differential Equations ◽  
Cell Population Growth ◽  
Chemotherapeutic Treatment ◽  
Stable Size Distribution ◽  
Distribution Theorem ◽  
Growth Of Tumor

A size-structured model is developed to study the growth of tumor cell populations during chemotherapeutic treatment with two non-cross resistant drugs, [Formula: see text] and [Formula: see text]. The cells reproduce by fission. Four types of cells are considered: sensitive cells to both [Formula: see text] and [Formula: see text], cells that are resistant to [Formula: see text] only, cells that are resistant to [Formula: see text] only, and cells that are resistant to both [Formula: see text] and [Formula: see text]. Resistant cells arise by spontaneous genetic mutation from sensitive cells and are selected during the growth of the mixed population. The model consists on a system of linear partial differential equations describing the size-density of each type of cells. That corresponds to chemotherapeutic treatment on a given time sequence intervals such that, we continuously apply [Formula: see text] at a first interval and next we apply [Formula: see text] at a second interval, and so forth. We obtain a stable size-distribution theorem for this case.

scholarly journals Butyrylcholinesterase Is Associated With β-Amyloid Plaques in the Transgenic APPSWE/PSEN1dE9 Mouse Model of Alzheimer Disease

2012 ◽  
Vol 71 (1) ◽  
pp. 2-14 ◽  
Author(s):  
Sultan Darvesh ◽  
Meghan K. Cash ◽  
George Andrew Reid ◽  
Earl Martin ◽  
Arnold Mitnitski ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Mouse Model ◽  
Amyloid Plaques ◽  
Β Amyloid

Astrocytes accumulate Aβ42 and give rise to astrocytic amyloid plaques in Alzheimer disease brains

2003 ◽  
Vol 971 (2) ◽  
pp. 197-209 ◽  
Author(s):  
Robert G. Nagele ◽  
Michael R. D’Andrea ◽  
H. Lee ◽  
Venkateswar Venkataraman ◽  
Hoau-Yan Wang
Keyword(s):  
Alzheimer Disease ◽  
Amyloid Plaques
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