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4 edition of The role of human kallikrein 6 in the pathogenesis of Alzheimer"s disease found in the catalog.

The role of human kallikrein 6 in the pathogenesis of Alzheimer"s disease

Maryam Zarghooni

The role of human kallikrein 6 in the pathogenesis of Alzheimer"s disease

by Maryam Zarghooni

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  • 11 Currently reading

Published by National Library of Canada in Ottawa .
Written in English


Edition Notes

Thesis (M.Sc.) -- University of Toronto, 2002.

SeriesCanadian theses = -- Th`eses canadiennes
The Physical Object
FormatMicroform
Pagination2 microfiches : negative.
ID Numbers
Open LibraryOL19897664M
ISBN 100612740471
OCLC/WorldCa54206083

Expression and Function of the Kallikrein-Related Peptidase 6 in the Human Melanoma Microenvironment Stefanie Krenzer1, Heike Peterziel1, Cornelia Mauch2, Sachiko I. Blaber3, Michael Blaber3, Peter Angel1 and Jochen Hess1,4,5 Cutaneous malignant melanoma is an aggressive disease of poor prognosis. Human Kallikrein 6 (hKLK6) is a member of tissue kallikrein family observed in breast and brain tissues, colon carcinoma cells, and oligodedrocytes (). Known protein substrates of hKLK6 are myelin basic protein, the precursor of the A beta amyloid peptide, and plasminogen.4/5(1).

  Alzheimer’s disease is a progressive mental deterioration. It can occur in middle or old age. It’s also one of the most common causes of premature senility in men and women. Two types of brain abnormalities define Alzheimer’s disease. They are Amyloid Plaques and Neurofibrillary Tangles. The accumulation of beta-amyloid [A β ] within senile plaques [SP] is characteristic of these lesions in Alzheimer’s disease. The accumulation of A β 42, in particular, in the superior temporal [ST] cortex may result from an inability of the blood brain barrier (BBB) to regulate the trans-endothelial transport and clearance of the by:

Alzheimer's disease/senile dementia of the Alzheimer type (AD/SDAT) is the most common neuropathologic substrate of dementia. It is characterized by synapse loss (predominantly within neocortex) as well as deposition of certain distinctive lesions (the result of protein misfolding) throughout the brain. The latter include senile plaques, composed mainly of an amyloid (Aβ) core and a neuritic Cited by: Kallikrein-related peptidase 6 (Klk6) is elevated in the serum of multiple sclerosis (MS) patients and is hypothesized to participate in inflammatory and neuropathogenic aspects of the by: 3.


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The role of human kallikrein 6 in the pathogenesis of Alzheimer"s disease by Maryam Zarghooni Download PDF EPUB FB2

Our transcriptomic study revealed an important upregulation of the Klk6 gene that encodes kallikrein-related peptidase 6, which is a biomarker of Alzheimer's disease (Diamandis et al., Any comprehensive theory of AD pathogenesis must explain the different pathologies observed in Alzheimer’s disease.

AD cybrids with reduced cytochrome oxidase activity overproduce Aβ42 and Aβ40 (Khan et al ). Under in vitro conditions sodium azide, a cytochrome oxidase inhibitor, alters APP processing towards amyloidogenic pathways Cited by:   Human herpes virus type 6 (HHV-6) has been suggested to be involved in the pathogenesis of AD as well.

This double stranded DNA virus can infect the brain [ 7, 8 ], and, interestingly, HHV as well asHSVassociated encephalitis, predominantly interest the fronto-temporal region of the brain: the same brain area that is most commonly Cited by: Background: The human kallikrein 6 gene (KLK6) encodes for a secreted serine protease, hK6, which is highly expressed in brain.

Previous reports have associated hK6 with the pathogenesis of Alzheimer’s disease. Our objective was to develop a highly sensitive immunoassay for hK6 and use it to examine the levels of hK6 in brain tissue extracts from Alzheimer’s disease patients and control Cited by: The human tissue kallikrein gene symbol is KLK1 [4].

Other human tissue kallikrein genes include KLK2 (human glandular kallikrein-1) and KLK3 (prostate-specific antigen or semenogelase).

The construction of a more detailed genomic map of the human tissue kallikrein locus showed that 15 genes share significant structural similarities [5,6]. The etiopathogenesis of the AD is unclear, but a role for viral infection is suspected to play a role in initiating the disease.

We recently described a positive correlation between high titers of HSVspecific antibodies (Ab) and the volumes of brain regions typically affected in by: Alzheimer's Disease: Advances in Etiology, Pathogenesis and Therapeutics will provide essential information for basic and clinical researchers in Alzheimer's Disease and other dementias as well as for those who care for patients.

Human kallikrein 8 (hK8), whose gene was originally cloned as the human ortholog of a mouse brain protease, is known to be associated with diseases such as ovarian cancer and Alzheimer's disease. Kallikrein 6 (KLK6) is known to be an age-related protease expressed at high levels in the central nervous system.

It was previously shown to be involved in proteolysis of extracellular proteins implicated in neurodegenerative diseases such as Alzheimer’s disease (AD), prompting validation of KLK6 as a potential biomarker of disease. However, analyses of both plasma and cerebrospinal fluid Cited by: 4.

in the known human kallikrein gene locus on chromosome 19qq (67–90). The recent detailed molecular descrip-tion of the human kallikrein gene locus (67, 68) enabled us to construct a physical map containing 15 genes that share TABLE 1.

Similarities between members of. Dodge HH, Zhu J, Woltjer R, et al. Risk of incident clinical diagnosis of Alzheimer's disease-type dementia attributable to pathology-confirmed vascular disease.

Alzheimers Dement ; Song Y, Stampfer MJ, Liu S. Meta-analysis: apolipoprotein E genotypes and risk for coronary heart disease. Title: Alzheimer Disease and the Role of Free Radicals in the Pathogenesis of the Disease VOLUME: 7 ISSUE: 1 Author(s):George Perry, Paula I.

Moreira, Maria S. Santos, Catarina R. Oliveira, Justin C. Shenk, Akihiko Nunomura, Mark A. Smith and Xiongwei Zhu Affiliation:College of Sciences, University of Texas at San Antonio, One UTSA Circle, San Antonio, Texas by:   While our understanding of the neuropathology of Alzheimer’s disease continues to grow, its pathogenesis remains a subject of intense debate.

Genetic mutations contribute to a minority of early-onset autosomal dominant cases, but most cases are of either late-onset familial or sporadic form.

CNS infections, most notably herpes simplex virus type 1, Chlamydophila pneumoniae and several Cited by:   Director of the USC Zilkha Neurogenetic Institute, Dr.

Berislav Zlokovic researches the pathogenesis or causes of Alzheimer's Disease, ALS (aka Lou Gehrig's Disease) and Strokes. Alzheimer’s disease (AD) is known as the most fatal chronic neurodegenerative disease in adults along with progressive loss of memory and other cognitive function disorders.

Cyclin-dependent kinase 5 (Cdk5), a unique member of the cyclin-dependent kinases (Cdks), is reported to intimately associate with the process of the pathogenesis of by:   Sharma, N. et al. Substrate specificity determination of mouse implantation serine proteinase and human kallikrein-related peptidase 6 by phage Cited by: The most influential theory to explain the pathogenesis of Alzheimer's disease (AD) has been the “Amyloid Cascade Hypothesis” (ACH) first formulated in The ACH proposes that the deposition of β -amyloid (A β) is the initial pathological event in AD leading to the formation of senile plaques (SPs) and then to neurofibrillary tangles (NFTs) death of neurons, and ultimately by:   Roher, A.

et al. Amyloid β peptides in human plasma and tissues and their significance for Alzheimer's disease. Alzheimers Dement. 5, 18–29 (). This study evaluates Aβ levels in brain Cited by: eBook/Print Book Bundle: This package includes an access code card for the eBook and the paperback textbook Introduction to Human Disease: Pathophysiology for Health Professionals, Sixth Edition provides a broad overview of the most common and important human diseases for students pursuing careers in the health professions/5(25).

Alzheimer’s Disease Pathogenesis: The Role of Aging Denham Harman, M.D., Ph.D.1 Abstract Alzheimer’s disease (AD) is character-ized by intraneuronal fibrillary tangles, plaques and cell loss.

Brain lesions in both sporadic AD (SAD) and familial AD (FAD) are the same, and in the same distribution pattern, as those in individuals with Down’s. Structures and specificity of the human kallikrein-related peptidases KLK 4, 5, 6, and 7 levels of which are associated with shorter disease-free and overall survival (Hoffman et al., ).

different role of KLK7 in these two tumor types. Aberrant KLK expression in tumor tissue may be due.Learn human disease pathophysiology with free interactive flashcards.

Choose from different sets of human disease pathophysiology flashcards on Quizlet.Evidence from epidemiological, neuroimaging, and neuropathological research, supports the role of genetic, vascular, and psychosocial factors in the development of Alzheimer’s disease, whereas evidence for the etiologic role of dietary or nutritional factors, occupational exposures, and Cited by: 7.