Erythropoietin and Epidemiology of Alzheimer Disease

  title={Erythropoietin and Epidemiology of Alzheimer Disease},
  author={Rovshan M. Ismailov},
  journal={Alzheimer Disease \& Associated Disorders},
  • R. M. Ismailov
  • Published 1 July 2013
  • Biology
  • Alzheimer Disease & Associated Disorders
Alzheimer disease (AD) is a neurodegenerative disorder with a strong vascular component and the most frequent form of dementia. The cause of AD is still not well understood. A number of hypotheses have been developed, yet the cause is still unknown. For example, the amyloid hypothesis suggested that the deposit of the b-amyloid peptide can lead to cognitive decline as well as to disrupted cerebral blood flow.1 However, some research evidence showed that older individuals can have extensive… 
The Role of Erythropoietin and its Receptor in the Immune , Central Nervous and Cardiovascular Systems
Current knowledge on the role of EPO and its receptor in the immune, central nervous and cardiovascular systems in various pathophysiological situations is presented.
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It was found that widths, antero-posterior lengths and volumes of frontal sinus were higher in populationsliving in colder climate and higher altitude according to populations living in mil der cli ate and lower altitude, appropriate to increasing of ephalic index in cold climate according to Allen’s Rule.
Foetal Adjustment to Precarious Conditions: Genes Elegantly Bioprocess
The objective of this perspective article was to underline the significance of embryonic and foetal adaptation to risky environmental conditions through internal maternal and own physiology. Mammals


Impaired cerebromicrovascular perfusion. Summary of evidence in support of its causality in Alzheimer's disease.
CATCH supports the heterogeneic disease profile assumed to be characteristic of the AD syndrome and introduces a normal but potentially menacing process that lowers cerebral blood flow in proportion to increased aging.
Impaired Cerebromicrovascular Perfusion: Summary of Evidence in Support of Its Causality in Alzheimer's Disease
CATCH supports the heterogeneic disease profile assumed to be characteristic of the AD syndrome, and is a self‐sustaining and progressive circulatory insufficiency that will destabilize neurons, synapses, neurotransmission, and cognitive function.
Alzheimer neuropathologic alterations in aged cognitively normal subjects.
It is demonstrated that the brains of a large percentage of cognitively normal, relatively well-educated individuals contain numerous degenerative changes and only a small percentage are relatively free of these changes.
Improvement of cognitive functions in chronic schizophrenic patients by recombinant human erythropoietin
Patients receiving rhEPO showed a significant improvement over placebo patients in schizophrenia-related cognitive performance (RBANS subtests, WCST-64), but no effects on psychopathology or social functioning.
Erythropoietin reduces perihematomal inflammation and cell death with eNOS and STAT3 activations in experimental intracerebral hemorrhage
The data suggests that EPO treatment in ICH induces better functional recovery with reducing perihematomal inflammation and apoptosis, coupled with activations of eNOS, STAT3 and ERK.
Angiogenesis and plasticity: role of erythropoietin in vascular systems.
Recognition of the multipotential attributes of EPO for vascular systems may further the progress of the development of therapeutic strategies to delay the onset of degenerative diseases.
The non‐haematopoietic biological effects of erythropoietin
  • M. Arcasoy
  • Biology, Medicine
    British journal of haematology
  • 2008
A series of recent studies suggest that endogenous Epo–EpoR signalling contributes to wound healing responses, physiological and pathological angiogenesis, and the body’s innate response to injury in the brain and heart.
Erythropoietin-mediated neuroprotection involves cross-talk between Jak2 and NF-κB signalling cascades
It is shown that preconditioning with EPO protects neurons in models of ischaemic and degenerative damage due to excitotoxins and consequent generation of free radicals, including nitric oxide, and this EPO effect may underlie neuroprotection mediated by hypoxic–ischaemic preconditionsing.