Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Air pollution & the brain: Subchronic diesel exhaust exposure causes neuroinflammation and elevates early markers of neurodegenerative disease
Neurodegenerative disorders, such as Huntington’s, Alzheimer’s, and
Parkinson’s diseases, affect millions of people worldwide and currently there
are few effective treatments and no cures for these diseases. Transgenic mice
expressing human transgenes for huntingtin, amyloid precursor protein, and
other genes associated with familial forms of neurodegenerative disease in
humans provide remarkable tools for studying neurodegeneration because
they mimic many of the pathological and behavioural features of the human
The chapters in this book review the latest advances in the molecular mechanisms of autophagy, highlighting some of the most challenging research topics. The focus is mainly on how this basic cell defense mechanism comes into play in various pathologies, including liver diseases, myopathies, infectious diseases, cancers and neurodegenerative diseases. In these diseases, the contradictory autophagy roles of cell survival versus cell death emphasize the necessity of taking into account this double-edged nature in future development of already promising, autophagy- modulating, therapies....
A large number of neurodegenerative diseases in humans result from pro-tein misfolding and aggregation. Protein misfolding is believed to be the
primary cause of Alzheimer’s disease, Parkinson’s disease, Huntington’s
disease, Creutzfeldt–Jakob disease, cystic fibrosis, Gaucher’s disease and
many other degenerative and neurodegenerative disorders.
Recent studies indicate that the dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) gene, which is located on chromosome
21q22.2 and is overexpressed in Down syndrome (DS), may play a signifi-cant role in developmental brain defects and in early onset neurodegenera-tion, neuronal loss and dementia in DS.
After the successful cloning of the first gene for a polyglutamine disease in
1991, the expanded polyglutamine tract in the nine polyglutamine disease
proteins became an obvious therapeutic target. Early hypotheses were that
misfolded, precipitated protein could be a universal pathogenic mechanism.
However, new data are accumulating on Huntington’s disease and other
polyglutamine diseases that appear to contradict the toxic aggregate
The therapeutic fields where stratified medicine is expected to take off first are oncology,
secondary complications of diabetes, cardiovascular diseases and neurodegenerative diseases.
Though, the development of stratified medicine is largely dependant of the identification and the
qualification of pertinent biomarkers in these areas. Regrettably, only a few studies on
biomarkers have proved to be sufficiently powered to detect differences among genetic variants
and/or the function of gene products.
This life-course approach is supported by a growing literature that documents
how many adult health conditions have their origins in childhood and are affected
by childhood risk, protective, and health-promoting influences.
dence demonstrates how prenatal and early childhood risks that interfere with
growth can increase the risk of ischemic heart disease, hypertension, obesity, and
diabetes. Early exposure to infections and environmental toxins increase the like-
lihood of cancer, hypertension and stroke, and neurodegenerative diseases.
Numerous authors proposed chapters on their work, and those presented here are the
fruit of those proposals. As editor of this book, it has been my pleasure to collaborate
with these many, fine contributing scientists. This text brings forth a great amount of
fresh information on the biogeography and ecology of poorly known taxa and
landscapes, and explores biogeographic processes not previously studied. The
assembled work is an anthology of issues in modern biogeography, with topics
ranging across regional to global spatial scales, and ecological to evolutionary
Oxidative stress state is involved in the aging process as well as in a vast array of
pathological conditions, including atherosclerosis, cardiovascular complications, diabetes,
cancer, and neuropsychiatric and neurodegenerative diseases.
Pulmonary hypertension is characterized by a mediator imbalance with a
predominance of vasoconstriction and cell proliferation involving all layers of the
vessel. The end result is an increase in pulmonary vascular resistance, increased
workload of the right ventricle, and right ventricular hypertrophy to maintain an
adequate flow. Subsequently, right ventricular dilatation ensues the signs and
symptoms of right heart failure occurence.
Among all the clinical indications for which radiologists, nuclear medicine physicians,
neurologists, neurosurgeons, psychiatrists (and others examining disorders of
the brain) order and read brain PET scans, demand is greatest for those pertaining
to dementia and related disorders. This demand is driven by the sheer prevalence of
those conditions, coupled with the fact that the differential diagnosis for causes of
cognitive impairment is wide and often difficult to distinguish clinically.
Senescence is a biological process that causes a progressive deterioration of structure and function of all organs chronologically. Recent studies have revealed the detailed molecular mechanisms of senescence using cell culture system and experimental organisms. It is thought that senescence is a potential cause for the development of various age-related disorders such as cancer, cardiovascular and neurodegenerative disorders.
Learners enrolled in all healthcare training programs need to have a basic understanding
of medical genetics so that they can successfully transition from students to clinicians.
The field of medical genetics is advancing at a fast pace and is becoming increasingly integral
to all aspects of medicine. This fact emphasizes the need for every practicing clinician
and faculty member to develop an in-depth knowledge of the principles of human genetics,
given that they are applicable to such a wide variety of clinical presentations.
Neurodegenerative disorders are associated with oxidative stress. Low den-sity lipoprotein (LDL) exists in the brain and is especially sensitive to oxi-dative damage. Oxidative modification of LDL has been implicated in
the pathogenesis of neurodegenerative diseases. Therefore, protecting LDL
from oxidation may be essential in the brain.
Huntington’s disease (HD) is an inherited neurodegenerative disorder characterized by cortico-striatal dysfunction and loss of glutamate uptake. At 7 weeks of age, R6/2 mice, which model an aggressive form of juvenile HD, show a glutamate-uptake deficit in striatum that can be reversed by treatment with ceftriaxone, a b-lactam antibiotic that increases GLT1 expression. Only at advanced ages ( 11 weeks), however, do R6/2 mice show an actual loss of striatal GLT1. Here, we tested whether ceftriaxone can reverse the decline in GLT1 expression that occurs in older R6/2s.
Parkinson’s disease is the second most common neurodegenerative disorder. The pathological hallmark of the disease is degeneration of midbrain dopaminergic neurons. Genetic association studies have linked 13 human chromosomal loci to Parkinson’s disease. Identification of gene(s), as part of the etiology of Parkinson’s disease, within the large number of genes residing in these loci can be achieved through several approaches, including screening methods, and considering appropriate criteria.
Idiopathic Parkinson’s disease (PD) is an age-dependent, neurodegenerative
disorder and is predominantly sporadic. Only 20–30% of patients have a positive
family history for PD with a complex mode of inheritance. In a few
extended families, the disease is inherited as an autosomal dominant trait. Linkage
to chromosome 4 was reported in a large Italian kindred multiply affected
by an early-onset form of PD (1). However, this finding was not replicated in a
sample of 94 Caucasian families by Scott et al. (2), or in 13 multigenerational
families by Gasser et al. (3)....
Dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A)
is a protein kinase with diverse functions in neuronal development and
adult brain physiology. Higher than normal levels of DYRK1A are associ-ated with the pathology of neurodegenerative diseases and have been impli-cated in some neurobiological alterations of Down syndrome, such as
Extracellular signal-regulated kinase (ERK) is a versatile protein kinase
that regulates many cellular functions. Growing evidence suggests that
ERK1⁄2 plays a crucial role in promoting cell death in a variety of neuro-nal systems, including neurodegenerative diseases.