A few words about AD

AD Dementia: The social function, the composite activities of the daily life are obstructed. This state is the threshold between memory changes and in one more cognitive factor.
Alzheimer’s Pathology: Senile Plaques and neurofibrillary tangles, loss of neuronal synapses, amyloid deficits in the vascular cerebral cortex.
Atypical AD: Progressive aphasia, Logopenic aphasia, frontal AD morphology and cortical atrophy at the posterior section. Also is supported from amyloidosis biomarkers in brain or CSF.
MCI: Individuals that abstain from the clinicobiological character of AD and also have measurable MCI. Those individuals may suffer from AD, but there is no evidence for AD.
Mixed AD: Incidents that validate the diagnostic AD requirements for typical AD and there are disorders such as cerebrovascular disease or Lewy Bodies disease.
Preclinical States of AD: This state includes an in vivo amyloidosis evidence of the brain, or individuals whose families have the autosomal dominant mutation of AD.
Prodromal AD: Clinical Symptoms, memory disorders, Hippocampal volume loss and biomarkers of CSF that lead to AD pathology.
Typical AD: Progressive memory loss, cognitive disorders and neuropsychiatric modifications.

The real etiology of Alzheimer’s disease (AD) is still unclear while several risk factors have been recognized to catalytically affect the early onset and the progression of the disease. According to latest studies [1], AD can be categorized according to risk factors, symptoms, and pathophysiological lesions into 8 different categories. Furthermore, these 8 categories can be analyzed in depth, by adding potential biomarkers in each category which have been proved to affect the severity of the disease [2-3].
While several attempts at reducing AD severity have been already presented mainly targeting the symptomatic treatment [4], there is still no holistic therapy that can effectively reverse AD. For many scientists and pharmaceuticals companies there are several and different treatment approaches like cholinesterase inhibitors, NMDA receptor antagonist, b-secretase inhibitors, c-secretase inhibitors, a-secretase stimulators, tau inhibitors, immunotherapy, naturaceuticals and nanodrugs [4],[5] even though the more secure solution seems to be the early diagnosis of brain lesions, pathophysiological alterations and obvious the case of early and secure prediction.
Bayesian Statistics constitutes an impressive tool for science and especially for Biomedical Informatics and Medical Decision Systems. Bayesian theory is based on probability theory and for several years, many supporters of the Classical approach are opposed to the Bayesian one, due to the weak approach of prior distribution through quantitative data analysis [6-7].
According to the following studies, we extract the most well-known biomarkers’ probabilities estimation for the different AD categories [8]-[21], that play significant roles in AD early onset and progression. Please fill your anonymous test results for the most known and accepted AD biomarkers and we will calculate the probability of AD presence in relation to these biomarkers, based on a complex discrete Bayesian model [3].

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[2] Matzavinos V, Alexiou A, Greig NH, Kamal MA, Biomarkers for Alzheimer’s disease diagnosis. Current Alzheimer Research, Bentham Science, in press (2016).
[3] Alexiou A, Matzavinos V, Greig NH, Kamal MA, A Bayesian model for the early prediction and diagnosis of Alzheimer’s disease (2017).
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[5] Soursou G, Alexiou A, Ashraf GMd, Siyal AA, Mushtaq G, Kamal MA, Applications of nanotechnology in diagnostics and therapeutics of Alzheimer’s and Parkinson’s disease, Current Drug Metabolism, Bentham Science, Current Drug Metabolism 16(8), 705-712 (2015).
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[8] Alzheimer’s Association Alzheimer’s Disease Facts and Figures Alzheimer’s & Dementia 2015 11(3):1-88 (2015).
[9] Alzheimer’s Association Dementia with Lewy bodies (2015)
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[12] Thomas DB Early-Onset Familial Alzheimer Disease,GeneReviews (2012)
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[14] Yves Christen Oxidative stress and Alzheimer disease American Society for Clinical Nutrition 71(2):621-629 (2000)
[15] J.C. de la Torre Alzheimer Disease as a Vascular Disorder Nosological Evidence 33(4):1152-62 (2002)
[16] Pratic D, Clark CM, Liun F, Lee VYM, Trojanowski JQ Increase of Brain Oxidative Stress in Mild Cognitive Impairmen A Possible Predictor of Alzheimer Disease 59(6) (2002)
[17] Hooper C, Meimaridou E, Tavassoli M, Melino G, Lovestone S, Killicka R p53 is upregulated in Alzheimer’s disease and induces tau phosphorylation in HEK293a cells 418(1):34-37 (2007)
[18] Chakrabarty P, Li A, Ceballos-Diaz C, Eddy JA, Funk CC, Moore B, DiNunno N, Rosario AM, Cruz PE, Verbeeck C, Sacino A, Nix S, Janus C, Price ND, Das P, GOLDE TE IL-10 Alters Immunoproteostasis in APP Mice, Increasing Plaque Burden and Worsening Cognitive Behavior Neuron (2015)
[19] Wang X, Su B, Lee Hg, Li X, Perry G, Smith MA, Zhu X Impaired Balance of Mitochondrial Fission and Fusion in Alzheimer’s Disease The Journal of Neuroscience 29(28): 9090-9103 (2009)
[20] Nanotechnology for Alzheimer’s disease detection and treatment, Amir Nazem and G.Ali Mansoori, Insciences J. 2011, 1(4), 169-193; doi:10.5640/insc.0104169
[21] Foskett JK, Muller M, Takano H, Mak DOD, Abel T, Coulter DA, Shilling D, Role of Calcium in Familial Alzheimer’s Disease Clarified in Penn Study, Pointing to New Therapeutic Option, The Journal of Neuroscience (2014)