Alzheimer?s Disease and Glucose Metabolism

Abstract

A few epidemiological studies give prove that sort 2 diabetes mellitus builds the danger of adding to Alzheimer's malady fundamentally. Both issue share certain irregular natural components, for example, hindered glucose digestion system, insulin resistance, expanded β-amyloid arrangement, oxidative anxiety, and the vicinity of cutting edge glycation finished items. This audit concentrates on glucose digestion system weakness as a typical clinical and biochemical highlight shared by Alzheimer's infection and sort 2 diabetes. With better learning of the normal atomic and cell pathways included in the movement of these two issue, analysts may have the chance to outline compelling restorative mediations to treat or control sort 2 diabetes mellitus and, therefore, defer the onset or movement of Alzheimer's ailment. The pathogenesis recently onset sporadic Alzheimer's ailment (AD) is accepted to result from complex collaborations between wholesome, natural, epigenetic and hereditary components. Among those elements, adjusted flowing cholesterol homeostasis, autonomous of the APOE genotype, keeps on being ensnared in mind statement of amyloid beta protein (Aβ) and the pathogenesis of AD. It is accepted that trafficking of amyloid beta forerunner protein (AβPP) into endolysosomes seems to assume a basic part in deciding amyloidogenic preparing of AβPP in light of the fact that this is accurately where two chemicals discriminatingly critical in AβPP digestion system are found; beta amyloid changing over catalyst (BACE-1) and gamma secretase enzyme.

Keywords

Alzheimer’s Disease; β-Amyloid Cognitive Impairment; Dementia; Hyperinsulinemia; Impaired Glucose Metabolism

Introduction

Alzheimer's illness (AD) is an issue that predominantly takes its toll on the elderly populace of the world with its worldwide pervasiveness near to 50% among 85 years and more established individuals. Then again, the number of inhabitants on the planet experiencing sort 2 diabetes mellitus (T2DM) at present is 150 million in view of a report by CDC and this number will move to 300 million by the year 2025 [1]. The Rotterdam consider in the year 1999 [2] and a few the study of disease transmission studies from that point forward have reported that T2DM fundamentally builds the danger for creating memory and intellectual debilitation, dementia and AD [3,4]. A few studies have reasoned that there is a 65% expanded danger for creating AD in diabetic patients contrasted with non-diabetes, sound people while different studies have exhibited that the danger of creating AD is multiplied in diabetic patients [5-10]. In like manner, a late group companion study from Cache County discovered AD patients more defenseless against creating T2DM than non-AD people, consequently making a nearby relationship in the middle of AD and T2DM [11-15]. As of late, there have been some clinical trials of antidiabetic medications going ahead in AD patients [16-19].

Alzheimer's disease (AD), the most well-known neurodegenerative issue of maturity, is portrayed clinically by a dynamic decrease in psychological capacity, and pathologically by loss of synaptic honesty, loss of neurons and the vicinity of amyloid plaques made out of amyloid beta (Aβ) protein and neuronal tangles made out of hyperphosphorylated tau [1,2]. Cerebrum affidavit of amyloid beta protein (Aβ), a proteolytic cleavage result of amyloid beta forerunner protein (AβPP) by the beta-site AβPP cleavage compound 1 (BACE1) and γ-secretase, keeps on being viewed as a critical pathogenic variable of AD [20-24]. All things considered, quality changes in AβPP and presenilin-1 can prompt moderately uncommon familial AD with right on time onset [25]. Nonetheless, the dominant part of AD cases is sporadic in nature and is late in onset. Presently, pathogenic systems in charge of sporadic AD stay indistinct, however are accepted to result from complex associations between healthful, natural, epigenetic and hereditary components [26-30]. Among these variables, lifted plasma LDL cholesterol speaks to a vigorous danger component for AD pathogenesis. Here, we will talk about the amyloidogenic handling of AβPP, quickly portray cholesterol homeostasis in the fringe and in the cerebrum, examine the linkage between raised levels of plasma LDL cholesterol and AD pathogenesis, and investigate the hidden systems with an emphasis on amyloidogenic preparing of AβPP.

Amyloidogenic Processing Of AβPP

Full-length AβPP, a universally communicated sort I transmembrane protein with to a great extent uncharacterized cell capacities is blended in the endoplasmic reticulum and is transported to the Golgi/trans-Golgi system mechanical assembly, where it experiences posttranslational adjustments and development. Once embedded into plasma films through secretory vesicles, AβPP can movement into endosomes by means of clathrin-ward endocytosis whereupon it can either be reused back to the cell surface or conveyed to lysosomes for conceivable corruption [31-35].

Trafficking of AβPP into endolysosomes seems to assume a basic part in deciding the degree to which AβPP digestion system is non-amyloidogenic or is amyloidogenic [31-37]. For the non-amyloidogenic pathway, AβPP in plasma films is divided by α-secretase to deliver sAPPα that is both neurotrophic and neuroprotective [8]. For the amyloidogenic pathway, once AβPP is disguised into the acidic environment of endolysosomes, amyloidogenic digestion system of AβPP is catalyzed by BACE-1 and γ-secretase [38-41]. Amyloidogenesis of endosome-determined Aβ is further affected by the capacity of Aβ debasement to be catalyzed by lysosomeoccupant cathepsins [13]. Remaining levels of Aβ can either amass in endolysosomes as intraneuronal Aβ or it can be experience exocytotic discharge into extracellular spaces where diffuse Aβ plaque can shape. In this way, amyloidogenesis can be improved by such elements as those that advance AβPP disguise [14], those that upgrade protein levels and/or exercises of BACE-1 and/ or γ-secretase [42-47], those that counteract AβPP reusing back to the cell surface [17], and those that impede Aβ destruction in lysosomes [48].

Cholesterol, a vital part of cellular membranes, helps keep up such physiologically imperative neuronal capacities as neurotransmitter discharge, neurite outgrowth, and synaptic pliancy [49-52]. Whether combined in mind or somewhere else all through the body, cholesterol is the same artificially. In any case, there are contrasts regarding its relationship with lipoprotein particles. Lipoproteins shift in size, lipid creation, and complex apolipoproteins that intercede their vehicle and uptake are diverse. In plasma, LDL is the fundamental lipoprotein molecule that intervenes the vehicle of cholesterol and lipids into fringe tissues, while HDL is the principle lipoprotein molecule that intercedes the converse cholesterol transport from fringe tissues [52-56]. LDL is a 20-25 nm measured molecule that has the most noteworthy cholesterol substance and apoB-100 is the select apolipoprotein that intervenes its vehicle and uptake. HDL, a protein-rich circle molded particles, is around 8-10 nm in size, has lower cholesterol substance, and essential apolipoproteins that intervene its vehicle and uptake are apoA-I, apoC-I, apoC-II and apoE [56-58].

Cerebrum is the most cholesterol rich organ in the body and contains around 20% of the body's aggregate cholesterol. Around 70% of mind cholesterol lies in the myelin sheaths of oligodendroglia and layers of astrocytes; cholesterol in neurons makes up the rest. Rather than plasma cholesterol, basically all cholesterol in the cerebrum is unesterified free cholesterol [58-61]. Such unesterifed free cholesterol is of specific significance to neurons on the grounds that neurons are remarkably energized cells with broad procedures that oblige steady film trafficking and free cholesterol reusing to keep up physiologically vital neuronal capacities, including neurotransmitter discharge, neurite outgrowth, and synaptic versatility [61-66].

HDL-like apoE-cholesterol incorporated in cerebrum supplies the neuronal need of cholesterol through receptor-interceded endocytosis, a procedure where lipoproteins bound to their receptors are disguised, transported to endolysosomes, hydrolyzed to free cholesterol, and from where free cholesterol is transported to different intracellular compartments (ER, Golgi) or plasma film by means of an instrument including the Niemann-Pick sort C (NPC) proteins sort 1 (NPC1) and -2 (NPC2) proteins [66-70]. To suit the neuronal requirement for cholesterol, countless for cholesterol uptake, including LDLR, low-thickness lipoprotein receptor (VLDLR), LRP-1, apoE receptor, and sorLA-1, are exceptionally communicated on neurons [32-35]. What's more, low levels of forager receptors B1 (SR-B1) and receptors for oxidized LDL are likewise communicated in neurons [36-38]. Hence, like that of plasma HDL, mind in situ incorporated HDL-like apoE-cholesterol may intervene reusing and opposite cholesterol transport [27], and such a capacity is particularly essential for central physiological elements of neurons. For sure, apoE is critical for the regulation of neurotransmitter development, versatility and repair [39,40] and apoE cholesterol, the nature wellspring of neuronal cholesterol, is neuroprotective [41,42]. Essentially, HDL is neuroprotective [43-45].

Butyrylcholinesterase (BChE) is expanded in the cerebral cortex of Alzheimer's Disease (AD) patients, especially those carryingå4 allele of the apolipoprotein E quality (ApoE) and certain BuChE variations that foresee expanded AD danger and poor reaction to anticholinesterase treatment. Measured BChE movement and protein level in CSF of eighty mellow AD patients in connection to age, sex, ApoE å4 genotype, cognizance and cerebral glucose digestion system (CMRglc). BuChE action was 23% higher in men than ladies (p < 0.03) and 40–60% higher in ApoE å4 negative patients than in those conveying maybe a couple å4 alleles (p < 0.0004). CSF BuChE level connected with cortical CMRglc. Patients with high to direct CSF BuChE demonstrated preferable intellectual capacity scores over others. They speculate that CSF BuChE shifts conversely with BuChE in cortical amyloid plaques. In this manner, low BuChE in a persistent's CSF may foresee far reaching consolidation in neuritic plaques, expanded neurotoxicity and more prominent focal neurodegeneration [71-75].

Interestingly, streptozotocin diabetes did not influence acetylcholinesterase action in the retina but rather expanded its movement in the cerebral cortex (100%) and in serum (55%), and diminished it by 30-40% in erythrocytes. The butyrylcholinesterase action was diminished by 30-50% in retina and hippocampus and to a lesser degree in retinal color epithelium from rats treated with streptozotocin for one week. The progressions noted in cholinesterase exercises were not related with the fasting blood glucose focus. These outcomes recommend that diabetes may impact a particular subset of cells and isoforms of cholinesterases that could prompt adjustments connected with diabetes difficulties. It was additionally reported that the butyrylcholinesterase K variation allele was more regular among Type II diabetic subjects than non-diabetic subjects recommending that the nearby relationship of the butyrylcholinesterase quality (3q26) with Type II diabetes could be identified with a recognized weakness locus on chromosome 3q27 yet free of islet capacity [76-78].

Glycation or a Maillard response is a post translational adjustment occasion which is the consequence of covalent holding of a free amino gathering of proteins with a diminishing sugar, for example, glucose and fructose which brings about the arrangement of an early glycation item that experiences revamp, drying out and cyclization to shape a more steady Amadori item (ketoamine) [1-4]. Both Schiff base and Amadori glycation items create free radicals bringing about decrease of cancer prevention agent protection instruments which can harm cell organelles and catalysts [5]. Under high glucose load (hyperglycaemic condition), the Amadori items experience a non-enzymatic glycation response prompting the development of an unpredictable arrangement of mixes known as the Advanced Glycation End items (AGEs) through middle of the road mixes, for example, 3-Deoxyglucosone (3DG), Glyoxal (GO) and Methylglyoxal MG [6]. Notwithstanding the way that sugars are the primary antecedents of AGEs, these gobetween metabolites are likewise accepted to take an interest in glycation responses [79-85]. Among these are 3-Deoxyglucosone (3-DG), known not an essential profoundly responsive dicarbonyl middle of the Maillard response; and Carboxymethyllysine (CML) and pentosidine as promoters of development of AGEs. These transitional mixes can likewise diffuse out of the cell and respond with extracellular proteins. Unreasonable AGE gathering results in huge cell brokenness by modifying protein structure. Subsequently, 3DG, GO and MG are glycation intermediates and antecedents of AGEs; and significant focuses for inhibitory mixes intended to decrease the undesirable results of protein glycation both in vitro and in vivo [86-90]. Notwithstanding proteins, glycation influences a mixture of different biomolecules containing free amino gatherings, for example, DNA and lipoproteins, accordingly annoying the structure and capacity of these biomolecules. The schematic representations of DNA glycation pathway alongside protein and lipid macromolecule is given in Scheme 1 [91-97].

The overwhelming calculate protein glycation is the half-existence of individual proteins; more noteworthy the half-life, bigger the glycation [8,9] The part of glycation turned out to be altogether mindful in numerous proteins for their basic disfigurement and their capacities [98-104]. The objective proteins are similar to; Immunoglobulin G (IgG), HSA, collagen which causes undesirable results. IgG and egg whites having half-existences of around 21 and 20 days, separately, display most extreme in vivo glycation. Then again, at high glucose focus, the degree of glycation is predominantly dictated by natural glycability of protein [104-110]. Glycation of Immunoglobulin G (IgG) has been embroiled in immune system illnesses, for example, Rheumatoid Arthritis (RA) [10]. This may meddle with the typical capacity of IgG and may add to start of ligament entanglements [110-117]. AGEs harmed IgG may be utilized as a biomarker for right on time location of RA and the related optional intricacies. Glycation of IgG is of exceptional enthusiasm because of its impact on the usefulness of immunoglobulin and general insusceptible fitness, particularly concerning their capacity to tie antigens and affect the supplement course [118]. Glycation of immunoglobulin has been demonstrated to bring about major auxiliary bothers bringing about their useful incapacity [10].

Another serum protein is Human Serum Albumin (HSA) which is exceedingly vulnerable to glycation. HSA is the most rich protein that contains 60% of human plasma protein. It has been utilized as a model protein for protein collapsing and ligand tying studies over numerous decades because of its long life period and high focus in plasma [118-122]. HSA is exceptionally delicate to glycation on the grounds that HSA bears roughly 58 Lys deposits, making it an ideal focus for the glycation process [11]. The level of glycated egg whites may additionally be of quality as a marker of the level of hyperglycaemia in diabetics [122-128].

Among the additional cell protein, collagen is the most essential one to experience glycation response. Collagens are critical proteins for the skin, as they are crucial for structure and capacity of the extracellular framework in the dermis. More slender and wrinkled skin, the average indications of ordinary maturing, is the outcome of decreased collagen [128-132]. Protein glycation particularly collagen, because of its long half-life, adds to skin maturing as it crumbles the current collagen by cross connecting [133].

Expanded glycation and manufacture up of tissue AGEs have been involved in diabetic entanglements in light of the fact that they can change enzymatic movement, diminish ligand tying, adjust protein half-life and modify immunogenicity. Some late studies have reported the vicinity of auto-antibodies against DNA and protein-AGEs in the serum of infected people [133-138]. AGEs are equipped for framing AGE-safe edifices in diabetic patients that may assume a part in atherogenesis. Glycation-inferred free radicals can bring about protein fracture and oxidation of nucleic acids and lipids. AGEs could likewise shape on phospholipids and prompt lipid peroxidation by an immediate response in the middle of glucose and amino gatherings on phospholipids, for example, phosphatidyl ethanolamine and phosphatidyl serine deposits [138-145].

The impact of glycation on lysine rich proteins and their inclusion in maturing and age-related sicknesses has been inspected circumspectly [145-151]. The proofs bolster antigenicity of the glycated lysine buildups in vivo with perception of auto-antibodies against the glycated proteins in diabetes and RA patients. This could be because of insurance of the changed proteins from proteolytic breakdown and its acknowledgment as a remote atom by the safe framework [152]. A more prominent comprehension of the regulation of glycated lysine items, particularly Amadori items, in maturing may assume an essential part in keeping the danger of age-related infections. Consequently, auto-antibodies to glycated proteins represent a marker for future age related infections in right away solid people [24]. Our exploration group has tested the vicinity of auto-antibodies against the cancer-causing agent/free radical and glycated DNA particle as a likely bio-marker for the recognition of right on time onset of the sicknesses like diabetes, joint inflammation and growth also [152-155].

The investigation of glycation gets to be vital in light of the fact that AGEs continuously amass on tissues and organs creating ceaseless inconveniences of diabetes, retinopathy, neuropathy and dynamic atherosclerosis [156].

Discussion

AD and T2DM are conditions that influence an expansive number of individuals in developed and developing nations. Both conditions are on the build, and discovering novel medicines to cure or forestall them are a real point in exploration. Somewhat surprisingly, AD and T2DM offer a few sub-atomic procedures that underlie the individual degenerative improvements performed the part of oxidative stretch in the pathogenesis of metabolic ailments like diabetes mellitus and its inconveniences, and also in neurodegenerative issue like AD and reported that the oxidative anxiety changes in the cerebrum of STZ-affected rats and people with AD could be valuable in the quest for new medications in the treatment of AD that have cancer prevention agent movement [157-164]. The misfolding of proteins assumes a vital part in both sicknesses, Our bioinformatic investigation conjecture that the nearby separation relationship in the middle of AChE and BChE may alter the danger for AD in people with T2DM. In a comparable in silico study directed by, exhibited that PhosphoBlast is an adaptable mining device fit for distinguishing related phosphorylation marks and phosphoamino corrosive transformations among complex proteomics datasets in a profoundly productive and precise way [165-171]. Phosphoblast will help in the informatics examination of the phosphoproteome and the recognizable proof of phosphoprotein biomarkers of illness. So bioinformatic studies like different arrangement and Phosphoblast investigation will help in the informatics examination of the protein and the distinguishing proof of new helpful intercessions/ protein biomarkers of the malady [172-176].

Expanded non-enzymatic protein glycation, development of AGEs and their amassing in tissue and serum have an essential part in the pathogenesis of diabetes difficulties. Long- lived extracellular proteins have highlighted the significance of intracellular glycation [177-180]. The synthetic way of AGEs, their blend in vivo and their exact part in the pathogenesis of diabetes muddling is under scrutiny. The diabetic entanglement can be lessened by decreasing glycation combination cross-join development and tissue collection of AGEs or by blocking AGEs receptors. As of late our gathering has focussed in the hindrance of AGEs utilizing potential medications like metformin and pyridoxamine [181-184]. Various common and manufactured mixes are being researched for their conceivable restorative potential having against oxidant potential [185-188]. We additionally estimated that therapeutic plants having against oxidant potential may likewise end up being have great hostile to glycation ability [52]. The mixes like, aminoguanidine counteract development of AGEs and have demonstrated promising in the avoidance of diabetic difficulties in creature models. On the other hand, they couldn't be created into a compelling attractive medication, because of security contemplations. Better comprehension of the sub-atomic component, in charge of diabetic complexities is fundamental for advancement of the inhibiters of AGEs [189-197].

Conclusion

Taking everything into account, organic systems basic to both AD and T2DM may give us an intimation to the advancement and movement of AD. At present, different restorative specialists have as of now been clinically demonstrated to avoid or deferral the onset of T2DM and AD and this clinical proof in itself affirms the relationship of T2DM and AD. Notwithstanding, there is still a need to further study the between associated cell and atomic instruments in the middle of T2DM and AD. Better comprehension of the disability of glucose digestion system as a pathophysiological connection in the middle of AD and T2DM is pivotal in light of the fact that this learning will control the scientists in outlining future restorative procedures focusing on both of the pathologies at the atomic level.

Raised levels of circling cholesterol, autonomous of APOE genotype, seem to add to the improvement of AD. On one hand, raised levels of plasma LDL cholesterol could advance cerebral vascular harm therefore starting neuroinflammatory reactions that add to the pathogenesis of AD. Then again, LDL cholesterol could aggravate neuronal endolysosome work and contribute straightforwardly to the pathogenesis AD. Here, we propose a speculation that hoisted levels of LDL cholesterol lead to lysosome cholesterol stockpiling like Niemann-Pick sort C infection in this way contributing the pathogenesis of AD. In particular, we recommend that plasma LDL cholesterol once it enters cerebrum parenchyma can be disguised by neurons through receptorinterceded endocytosis and can advances AβPP disguise in light of the fact that LDLRs and AβPP physically take up with one another. Dissimilar to apoE-cholesterol, expanded apoB-containing LDL-cholesterol could prompt cholesterol amassing in endolysosomes along these lines raising endolysosome pH and impeding endolysosome capacity.

Rise of endolysosome pH on one hand could prompt expanded BACE-1 protein levels and upgraded BACE-1 movement that prompts amyloidogenic preparing of AβPP, and then again could decrease cathepsin action subsequently weakening Aβ debasement in lysosomes, hence prompting intraneuronal Aβ amassing. Despite the fact that discoveries from our creature studies backing such a theory, further studies directed in people are justified. It additionally ought to be observed that cholesterol is by all account not the only part of LDL particles and related apolipoproteins, sphingolipids and phospholipids could likewise influence amyloidogenic handling of AβPP and add to the improvement of sporadic AD.

While the recognizable proof of these hopeful proteins included in AD and T2DM is an essential in silico breakthrough, catch up studies are needed for acceptance in a bigger populace of people and for determination of lab characterized affectability and specificity qualities utilizing novel proteomic and metabolomic devices. The mix of proteomic and bioinformatic studies are valuable for more exact forecast of biomarkers/new therapeutic targets.

References

1. Singh SK, et al. Structure modeling and dynamics driven mutation and phosphorylation analysis of Beta-amyloid peptides. Bioinformation. 2014; 30: 569-574.
2. Nichols TW , et al. Hyperphosphorylation of Tau Protein in Down’s Dementia and Alzheimer’s Disease: Methylation and Implications in Prevention and Therapy J Alzheimers Dis Parkinsonism.2014; 4: 159.
3. Ildefonso RL, et al. Presence of Phosphorylated Tau Protein in the Skin of Alzheimer´s Disease Patients J Mol Biomark Diagn S.2015; 6: 005.
4. Tsai A, et al. Differences in Cerebrospinal Fluid Biomarkers between Clinically Diagnosed Idiopathic Normal Pressure Hydrocephalus and Alzheimer’s Disease J Alzheimers Dis Parkinsonism.2014; 4: 150.
5. Reiber H, et al. Neurochemical Dementia Diagnostics – Interlaboratory Variation of Analysis, Reference Ranges and Interpretations J Alzheimers Dis Parkinsonism.2014; 4: 147.
6. Shin HW, et al. Differences in BDNF Serum Levels in Patients with Alzheimer’s Disease and Mild Cognitive Impairment J Psychiatry.2015; 18: 245
7. Pasha EP, et al. Ethnoracial Disparities in Alzheimer’s Disease: Target on Cardiovascular Risks via Lifestyle Changes? J Gerontol Geriat Res.2014; 3: 128.
8. Ressner P, et al. Computer-Assisted Cognitive Rehabilitation in Stroke and Alzheimer’s disease J Neurol Neurophysiol.2014; 5: 260.
9. Park AL , et al. Is There Anything Special About Intergenerational Approaches to Older People with Dementia? A Review J Alzheimers Dis Parkinsonism.2014; 4: 172.
10. Miyaoka T, et al. Effect of Donepezil on Sleep and Activity in Alzheimer’s Disease: Actigraphic and Polysomnographic Assessment J Alzheimers Dis Parkinsonism.2014; 4: 157.
11. Hanby MF, et al. Emotional and Cognitive Processing Deficits in People with Parkinson ’s Disease and Apathy J Alzheimers Dis Parkinsonism.2014; 4: 156.
12. Camargo CHF, et al. Orthostatic Hypotension and its Relationship to the Clinical Course of Patients with Parkinson’s Disease J Alzheimers Dis Parkinsonism.2014; 4: 155.
13. Davey DA , et al. Alzheimer’s Disease, Cerebrovascular Disease and Dementia: A Potentially Preventable and Modifiable Syndrome J Alzheimers Dis Parkinsonism.2015; 5: 184.
14. Sani M, et al. Successful Regeneration of CNS Nerve Cells a Possible Bye Bye O Debilitating Effects Of Neurodegenerative Diseases J Alzheimers Dis Parkinsonism.2015; 5: 182.
15. Stephenson D, et al. Alzheimer’s and Parkinson’s Diseases Face Common Challenges in Therapeutic Development: Role of the Precompetitive Consortium, Coalition Against Major Diseases J Alzheimers Dis Parkinsonism.2015; 5: 183.
16. Devasena T and Francis a A.P , et al. Nanotoxicity-Induced Alzheimer Disease and Parkinsonism: Not Further than Diagnosis J Alzheimers Dis Parkinsonism.2015; 5: 178.
17. Lukiw WJ, et al. Microbial Sources of Amyloid and Relevance to Amyloidogenesis and Alzheimer’s Disease.2015;
18. Jana P, et al. Epidemiology and Genetics of Alzheimer’s Disease J Alzheimers Dis Parkinsonism.2015; 5: 172.
19. Gareri P, et al. The Role of Quetiapine in the Treatment of Alzheimer's Disease J Gerontol Geriatr Res.2015; 4: 197
20. Miller MD, et al. Preparing for the Rise in Alzheimers Disease Cases: A Proposal for Training Support Personnel J Gerontol Geriatr Res.2015; 4: 195.
21. Kim H, et al. A Voxel-Based Morphometry Study in Alzheimer’s Disease and Mild Cognitive Impairment J Psychiatry.2015; 18: 237.
22. Ramdani L, et al. Multifunctional Curcumin-Nanocarriers Based on Host-Guest Interactions for Alzheimer Disease Diagnostic J Nanomed Nanotechnol.2015; 2015, 6: 270
23. RodriacuteguezLeyva Ildefonso, et al. Presence of Phosphorylated Tau Protein in the Skin of Alzheimer´s Disease Patients J Mol Biomark Diagn.2015; 2015, S6: 005
24. Lara Hvidsten, et al. Young Onset Dementia study – A Prospective Cohort Study of Quality of Life and Specific Needs in Persons with Young Onset Dementia and their Families J Clin Trials.2015; 2014, 5: 204
25. Evan P Pasha, et al. Ethnoracial Disparities in Alzheimer’s Disease: Target on Cardiovascular Risks via Lifestyle Changes? J Gerontol Geriatr Res.2014; 2014, 3: e128
26. FelixMartin Werner and Rafael Coventildeas, et al. Might Combined GABAA Agonists and NMDA Antagonists have a Therapeutic and maybe a Prophylactic Effect in Alzheimer's and Parkinson's Disease? J Cytol Histol.2015; 2015, 6: 298
27. Knarik Arkun, et al. Effect of Lewy Bodies on Mitochondrial DNA Copy Numbers and Deletion Burden in Parkinson’s Disease Substantia nigra Neurons J Alzheimers Dis Parkinsonism.2015; 2015, 4: 175
28. Orwa Aboud and Sue T. Griffin W, et al. Silver Staining of Alzheimer's Disease J Neurol Disord.2014; 2014, 2: i103
29. Pavel Ressner, et al. Computer-Assisted Cognitive Rehabilitation in Stroke and Alzheimer’s disease J Neurol Neurophysiol,.2014; 5: 260
30. Pranami Bhaumik, et al. A Rare Intronic Variation of Presenilin-1.2014; 1
31. Astrid Haram, et al. Clinical Correlates of RBD in Early Parkinson Disease J Alzheimers Dis Parkinsonism.2014; 2014, 4: 174
32. Hascalovici J and Schipper HM, et al. HemeOxygenase-1: Transducer of Sterol Dys-Regulation in Alzheimer Disease J Glycomics Lipidomics.2014; 1: Transducer of Sterol Dys-Regulation in Alzheimer Disease. J Glycomics Lipidomics 2014, 4: 124
33. Victoria I Bunik, et al. Benefits of Thiamin.2014;
34. ALa Park, et al. Is There Anything Special About Intergenerational Approaches to Older People with Dementia? A Review J Alzheimers Dis Parkinsonism.2014; 2014, 4: 172
35. Hyun Kim, et al. Differences in C-reactive Protein Level in Patients with Alzheimers Disease and Mild Cognitive Impairment J Psychiatry.2015;
36. David R. Borchelt, et al. Proteostasis and Secondary Proteinopathy in Alzheimer’s Disease J Alzheimers Dis Parkinsonism.2014; 2014, 4: 145
37. Vanessa K Hinson, et al. Forced Exercise for Freezing of Gait in Post STN DBS Parkinson’s Disease Patients J Alzheimers Dis Parkinsonism.2014; 2014, 4: 171
38. Borroni B, et al. Diagnosing Progressive Supranuclear Palsy: Role of Biological and Neuroimaging Markers J Alzheimers Dis Parkinsonism.2014; 2014, 4: 168
39. Keiko Ikemoto, et al. Lectin-Positive Spherical Deposits.2014;
40. Xu Xin, et al. The Hopkins Verbal Learning Test and Detection of MCI and Mild Dementia: A Literature Review J Alzheimers Dis Parkinsonism.2014; 2014, 4: 166
41. Robin Altman, et al. The Postprandial Effects of a Moderately High-Fat Meal on Lipid Profiles and Vascular Inflammation in Alzheimer’s Disease Patients: A Pilot Study J Gen Pract.2014; 2014, 2: 186
42. Paul Whitesman, et al. Preliminary Set Theory-Type Analysis of Proteins Associated With Parkinson’s Disease J Alzheimers Dis Parkinsonism.2014; 2014, 4: 170
43. Raheel Mushtaq, et al. Comparison of Cognitive Symptoms in Subtypes of Alzheimer’s disease.2014;
44. Servello A, et al. Role of Cardiovascular Comorbidity and Depressive Symptoms on One-Year Clinical Progression of Alzheimer’s Disease.2014;
45. Roberta Ciuffini, et al. Visual Evoked Potentials in Alzheimer's Disease: Electrophysiological Study of the Visual Pathways and Neuropsychological Correlates J Alzheimers Dis Parkinsonism.2014; 2014, 4: 158
46. Carrie A Ciro, et al. Improving Daily Life Skills in People with Dementia: Testing the STOMP Intervention Model J Alzheimers Dis Parkinsonism.2014; 2014, 4: 165
47. Travis H Turner, et al. Epidermal Growth Factor.2014;
48. Yellamma K, et al. Silk Protein, Sericin as a Cognitive Enhancer in Alzheimer’s Disease J Alzheimers Dis Parkinsonism.2014; 2014, 4: 163
49. Tiwari SC and Soni RM, et al. Alzheimer’s Disease Pathology and Oxidative Stress: Possible Therapeutic Options J Alzheimers Dis Parkinsonism.2014; 2014, 4: 162
50. Barbara Cynthia Fisher , et al. The Benefits of Cognitive Stimulation or Training/Rehabilitation upon Brain Function as an Efficacious Treatment for Diagnosed Dementia or Mild Cognitive Decline J Alzheimers Dis Parkinsonism.2014; 2014, 4: 161
51. Faris Yaghmoor, et al. The Role of TREM2 in Alzheimer’s Disease and Other Neurological Disorders J Alzheimers Dis Parkinsonism.2014; 2 in Alzheimer’s Disease and Other Neurological Disorders. J Alzheimers Dis Parkinsonism 2014, 4: 160
52. Tsuyoshi Miyaoka, et al. Effect of Donepezil on Sleep and Activity in Alzheimer’s Disease: Actigraphic and Polysomnographic Assessment J Alzheimers Dis Parkinsonism.2014; 2014, 4: 157
53. Martha F Hanby, et al. Emotional and Cognitive Processing Deficits in People with Parkinson’s Disease and Apathy J Alzheimers Dis Parkinsonism.2014; 2014, 4: 156
54. Carlos Henrique Ferreira Camargo, et al. Orthostatic Hypotension and its Relationship to the Clinical Co urse of Patients with Parkinson’s Disease J Alzheimers Dis Parkinsonism.2014; 2014, 4: 155 
55. Junseong Park, et al. Evaluation and Identification of Protein Blood Biomarkers for Alzheimer’s Disease: A Systematic Review and Integrative Analysis J Mol Biomark Diagn.2014; 2014, 5: 190
56. Amir Nazem, et al. Alzheimer’s Disease Drug Discovery may be Misled by Wrong Animal Models J Gerontol Geriatr Res.2014; 2014, 3: e127
57. Joan HQ Shen, et al. Validation of an Alzheimer’s Disease Assessment Battery in Asian Participants With Mild to Moderate Alzheimer’s Disease J Gerontol Geriatr Res.2014; 2014, 3: 167
58. Mi Tian, et al. Alzheimer’s Disease and Dementia, Under-Recognized Public Health Crisis in China J Gerontol Geriatr Res.2014; 2014, 3: 179
59. VandeWeerd C, et al. Changes in Conflict Resolution Style over Time: The Risk for Persons with Alzheimer's Dementia Aging Sci.2014; 2014, 2: 127
60. Xuesong Chen, et al. Role of LDL Cholesterol and Endolysosomes in Amyloidogenesis and Alzheimer’s Disease J Neurol Neurophysiol.2014; 2014, 5: 236
61. Koji Terasawa, et al. Relevance between Alzheimer’s Disease Patients and Normal Subjects Using Go/No-Go Tasks and Alzheimer Assessment Scores J Child Adolesc Behav.2014; 2014, 2: 162
62. James Oluwagbamigbe Fajemiroye, et al. Alzheimer’s Disease and Animal Models in Retrospect Med chem.2014; 2014, 4: 701
63. Hiroaki Tanaka, et al. Relationship with Bipolar Temperament and Behavioral and Psychological Symptoms of Dementia in Alzheimer’s Disease Brain Disord Ther.2014; 2014, 3: 144
64. Emanuela Onofri, et al. Cognitive Performance Deficits and Dysgraphia in Alzheimer’s Disease Patients J Neurol Neurophysiol.2014; 2014, 5: 223
65. Aryal R, et al. Is the A-beta peptide of Alzheimer’s Disease an Antimicrobial Peptide? J Gerontol Geriatr Res.2014; 2014, 3: 165
66. Christian Barbato, et al. Alzheim.2014;
67. Shephali Bhatnagar, et al. Compatible Changes of Lead microRNAs in Circulating Plasma and Brain in Senescence-Accelerated Aging and Alzheimer's disease Mouse Models Aging Sci.2014; 2014, 2: 125
68. Cacabelos R, et al. The Pathogenic Component of the APOE-TOMM40 Region in Alzheimer’s disease: Its Implications in Metabolomics and harmacogenomics Metabolomics.2014; 40 Region in Alzheimer’s disease: Its Implications in Metabolomics and harmacogenomics. Metabolomics 2014, 4: e129
69. Nazem A, et al. Nanotechnology Building Blocks for Intervention with Alzheimer’s Disease Pathology: Implications in Disease Modifying Strategies J Bioanal Biomed.2014; 2014
70. Jacques Hugon, et al. Involvement of PKR in Alzheimer’s Disease J Alzheimers Dis Parkinsonism.2014; 2014, 4: 154
71. Garth F Hall, et al. Report from the Tau Front: Cantoblanco 2013 J Alzheimers Dis Parkinsonism.2014; 2013. J Alzheimers Dis Parkinsonism 2014, 4: e133
72. Moretti DV, et al. Impairment of the Posterior Part of the Mirror Neurons System in Alzheimer’s Disease: Evidence from EEG Biomarkers J Alzheimers Dis Parkinsonism.2014; 2014, 4: 153
73. Jeroen J.M. Hoozemans, et al. Increased IRAK-4 Kinase Activity in Alzheimer’s Disease2014 4 Kinase Activity in Alzheimer’s Disease; IRAK-1/4 Inhibitor I Prevents Pro-inflammatory Cytokine Secretion but not the Uptake of Amyloid Beta by Primary Human Glia. J Clin Cell Immunol 2014, 5: 243
74. Balachandar Rakesh, et al. A Retrospective Study on Relation between Cognitive Performance and Lobar Perfusions of Brain in Alzheimer’s Dementia using Single Photon Emission Computer Tomography Brain Disord Ther.2014 2014, 3: 135
75. Kentaro Horiuchi, et al. Rivastigimine for Relatively Younger Alzheimer’s Disease Patient Brain Disord Ther.2014 2014, 3: 133
76. Jacques Hugon, et al.  Involvement of PKR in Alzheimer’s Disease. J Alzheimers Dis Parkinsonism.2014; 4: 154.
77. Garth F Hall, et al.  Report from the Tau Front: Cantoblanco 2013. J Alzheimers Dis Parkinsonism. 2014; 4: e133.
78. Moretti DV, et al.  Impairment of the Posterior Part of the Mirror Neurons System in Alzheimer’s Disease: Evidence from EEG Biomarkers. J Alzheimers Dis Parkinsonism. 2014; 4: 153.
79. Jeroen J.M. Hoozemans, et al.  Increased IRAK-4 Kinase Activity in Alzheimer’s Disease; IRAK-1/4 Inhibitor I Prevents Pro-inflammatory Cytokine Secretion but not the Uptake of Amyloid Beta by Primary Human Glia. J Clin Cell Immunol. 2014; 5: 243.
80. Balachandar Rakesh, et al.  A Retrospective Study on Relation between Cognitive Performance and Lobar Perfusions of Brain in Alzheimer’s Dementia using Single Photon Emission Computer Tomography. Brain Disord Ther. 2014; 3: 135.
81. Kentaro Horiuchi, et al.  Rivastigimine for Relatively Younger Alzheimer’s Disease Patient. Brain Disord Ther. 2014; 3: 133.
82. Scott J Weiland and Michelle Schmude, et al.  Student Athletes’ Perceptions of Concussions through Media Consumption. J Mass Communicat Journalism. 2014; 4: 199.
83. Ramoacuten Cacabelos, et al.  APOE-TOMM40 in the Pharmacogenomics of Dementia. J Pharmacogenomics Pharmacoproteomics. 2014; 5: 3.
84. Andrew Tsai, et al.  Differences in Cerebrospinal Fluid Biomarkers between Clinically Diagnosed Idiopathic Normal Pressure Hydrocephalus and Alzheimer’s Disease. J Alzheimers Dis Parkinsonism. 2014; 4: 150.
85. Hanaa L Sadek, et al.  The Inflammatory Cytokines in the Pathogenesis of Parkinson’s Disease. J Alzheimers Dis Parkinsonism. 2014; 4: 148.
86. Xudong Huang, et al.  Metal Exposure and Alzheimer’s Pathophysiology. Biochem & Pharmacol. 2014; 3: e156.
87. Pawe Szymaski, et al.  Diagnosis of Alzheimer Disease– The Most Popular and Future Perspective Methods. Biochem & Pharmacol. 2014; 3: e159.
88. Gandotra S, et al.  Efficacy of Adjunctive Extra Virgin Coconut Oil Use in Moderate to Severe Alzheimer’s Disease. Int J Sch Cog Psychol. 2014; 1: 108.
89. Karam A Mahdy, et al.  Protective Effect of Ginger..2014;.
90. Perez Martinez David Andres and Manzano Palomo Maria Sagrario, et al.  Trem2 Variants and Risk of Alzheimer’s Disease. Brain Disord Ther. 2014; 3: 127.
91. Daniel Paris, et al.  Anatabine Attenuates Tau Phosphorylation and Oligomerization in P301S Tau Transgenic Mice. Brain Disord Ther. 2014; 3: 126.
92. Miki Umetsu, et al.  Circadian Rhythm Sleep Disorder in Alzheimer’s Disease-A consideration in relation with the Neuropathological and Neuroendocrinal alternation-. Brain Disord Ther. 2014; 3: 124.
93. Maria Elisa de Oliveira Lanna, et al.  Diabetes Effects in Alzheimer Disease: The Interactive Role of Insulin and Aβ Peptide. J Alzheimers Dis Parkinsonism. 2014; 4: 151.
94. David Truswell, et al.  Black, Asian and Minority Ethnic Communities and Dementia – Where Are We Now?. J Alzheimers Dis Parkinsonism. 2014; 4: 152.
95. Hansotto Reiber, et al.  Neurochemical Dementia Diagnostics – Interlaboratory Variation of Analysis, Reference Ranges and Interpretations. J Alzheimers Dis Parkinsonism. 2014; 4: 147.
96. Florindo Stella, et al.  Neuropsychiatric Symptoms in Alzheimer’s Disease Patients: Improving the Diagnosis. J Alzheimers Dis Parkinsonism. 2014; 4: 146.
97. Pierre A. Denis , et al.  The Continuum of Metabolic Stress According to the Gas Model of Alzheimer’s Disease. J Alzheimers Dis Parkinsonism. 2014; 4: 149.
98. Krikor Dikranian and David M. Holtzman, et al.  The Ultrastructural Identity of Alzheimer’s Pathology: Lessons from Animal Models. J Neurol Disord. 2014; 2: e111.
99. Mitchell Clionsky and Emily Clionsky, et al.  Dementia Screening: Saying No to the USPSTF and Yes to Brief Cognitive Evaluation. J Alzheimers Dis Parkinsonism. 2014; 4: e132.
100. Shokouhi S, et al.  Imaging Brain Metabolism and Pathology in Alzheimer ’s Disease with Positron Emission Tomography. J Alzheimers Dis Parkinsonism. 2014; 4: 143.
101. Deacon RMJ , et al.  A Novel Approach to Discovering Treatments for Alzheimer ’s Disease. J Alzheimers Dis Parkinsonism. 2014; 4: 142.
102. Frank O Bastian , et al.  Cross-Roads in Research on Neurodegenerative Diseases. J Alzheimers Dis Parkinsonism. 2014; 4: 141.
103. Abraham Lieberman, et al.  Comparison of Parkinson Disease Patients Who Fell Once with Patients Who Fell More than Once. 2014.
104. Tetsumori Yamashima, et al.  Calpain-Mediated Hsp70..2014;.
105. Munvar Miya Shaik , et al.  Enzymes as Therapeutic Agents in Alzheimer’s Disease. J Biomol Res Ther. 2014; 3: e129.
106. Ramoacuten Cacabelos and Francisco LoacutepezMuntildeoz , et al.  The ABCB1 Transporter in Alzheimer’s Disease. Clin Exp Pharmacol. 2014; 4: e128.
107. Aaron Block, et al.  Abnormal Protein Profiles in Hippocampus of Mouse Models of Down Syndrome: Similarities with Alzheimers Disease. J Alzheimers Dis Parkinsonism. 2014; 4: 138.
108. Mark H Sundman, et al.  Examining the Relationship between Head Trauma and Neurodegenerative Disease: A Review of Epidemiology, Pathology and Neuroimaging Techniques. J Alzheimers Dis Parkinsonism. 2014; 4: 137.
109. Feasibility and Effectiveness of Balance and Gait Training Using Nintendo Wii Fit Plus™ on Unstable Surface in Patients with Parkinson’s Disease: A Pilot Study. J Alzheimers Dis Parkinsonism 2014.
110. Kurt A Jellinger , et al.  Neuropathology of Dementia Disorders. J Alzheimers Dis Parkinsonism. 2014; 4: 135.
111. Helmut Barz, et al.  Neuronal Impulse Theory and Alzheimer’s Disease. J Alzheimers Dis Parkinsonism. 2014; 4: 134.
112. Bajic P Vladan , et al.  Controversy in its Essence: The Alzheimer's Paradigm in Clinical Diagnosis and Research. JBR Journal of Clinical Diagnosis and Research.2013;.
113. Mak Adam Daulatzai , et al.  Obesity and Gut’s Dysbiosis Promote Neuroinflammation, Cognitive Impairment, and Vulnerability to Alzheimer’s disease: New Directions and Therapeutic Implications.  J Mol Genet Med. 2014; S1: 005.
114. Hyperhomocysteinemia and Gestational Programming of Genes Involved in Alzheimer’s Disease Pathogenesis. J Nutr Food Sci 2014, et al...;.
115. Agnes PirkerKees, et al.  T-Cells Show Increased Production of Cytokines and Activation Markers in Alzheimer’s Disease. Brain Disord Ther. 2014; 3: 112.
116. Surgery under Propofol Anesthesia Induced Behavioral Changes Associated With Increased Cerebral Apoptosis in Rats. J Liver 2013.
117. Kebreten F Manaye and William Rebeck G , et al.  Possible APOE Genotype and Sex Dependent Effects of 17-α- estradiol on Alzheimers Disease Pathology. J Alzheimers Dis Parkinsonism. 2013; 3: e130.
118. Jinichi Ito, et al.  Oxidative Stress and FGF-1 Release from Astrocytes. J Alzheimers Dis Parkinsonism. 2014; 4: 133.
119. Ashraf Virmani, et al.  Neuronal Carnitine Palmitoyl Transferase1c in the Central Nervous System: Current Visions and Perspectives. J Alzheimers Dis Parkinsonism. 2014; 4: 132.
120. Keith A Wesnes and David J Burn , et al.  Compromised Object Pattern Separation Performance in Parkinson′s Disease Suggests Dentate Gyrus Neurogenesis may be Compromised in the Condition. J Alzheimers Dis Parkinsonism. 2014; 4: 131.
121. AguirreRueda D, et al.  Pro-Oxidant and Inflammatory Mediators Produced In Transgenic Mice.
122. Fabiano Henrique Rodrigues Soares, et al.  Measures of Heart Rate Variability in Patients with Idiopathic Parkinson’s Disease. J Alzheimers Dis Parkinsonism. 2013; 3: 130.
123. Benjamin Schmitt, et al.  Quantitative Assessment of Metabolic Changes in the Developing Brain of C57BL/6 Mice by In Vivo Proton Magnetic Resonance Spectroscopy. J Alzheimers Dis Parkinsonism. 2013; 3: 129.
124. Sarah Lee, et al.  CSF and Brain Indices of Insulin Resistance, Oxidative Stress and Neuro-Inflammation in Early versus Late Alzheimer’s Disease. J Alzheimers Dis Parkinsonism. 2013; 3: 128.
125. Danielle Meola, et al.  Selective Neuronal and Brain Regional Expession of IL-2 in IL2P 8-GFP Transgenic Mice: Relation to Sensorimotor Gating. J Alzheimers Dis Parkinsonism. 2013; 3: 127.
126. SIRT1 Protects Dendrites, et al...;.
127. BradleyWhitman MA and Lovell MA , et al.  Increased Oxidative Damage in RNA in Alzheimer’s Disease Progression. J Anal Bioanal Tech. 2014; S2: 004.
128. Gabriela Beatriz Acosta , et al.  In Search of the Mysterious Alzheimer’s Disease. Clin Exp Pharmacol. 2012; S6: 001.
129. Sachiko Yokoyama, et al.  Escitalopram for Delusion in an Oldest Old Patient with Alzheimer’s Disease. Brain Disord Ther. 2013; 2: 108.
130. Mohit Jain, et al.  Data Adaptive Rule-based Classification System for Alzheimer Classification. J Comput Sci Syst Biol. 2013; 6: 291-297.
131. Ryan T Pitman, et al.  FTO Knockdown Decreases Phosphorylation of Tau in Neuronal Cells; A Potential Model Implicating the Association of FTO with Alzheimer’s Disease. J Alzheimers Dis Parkinsonism. 2013; 3: 125.
132. Koji Hori, et al.  Mini Review: Pharmacotherapy for Behavioral and Psychological Symptoms in Alzheimer?s Disease. Brain Disord Ther. 2013; 2: 106.
133. Pradeep Chowriappa, et al.  An Exploratory Analysis of Conservation of Co-Expressed Genes across Alzheimer's disease Progression. J Comput Sci Syst Biol. 2013; 6: 215-227.
134. Jun Iwamoto and Yoshihiro Sato , et al.  Strategy for Prevention of Hip Fractures in Patients with Alzheimer's Disease. General Med. 2013; 1: 114.
135. Rodrigo D Perea, et al.  A Comparative White Matter Study with Parkinson′s disease,Parkinson′s Disease with Dementia and Alzheimer′s Disease. J Alzheimers Dis Parkinsonism. 2013; 3: 123.
136. Fabian Fernandez and Jamie O Edgin, et al.  Poor Sleep as a Precursor to Cognitive Decline in Down Syndrome : A Hypothesis. J Alzheimers Dis Parkinsonism. 2013; 3: 124.
137. Ramon Casanova, et al.  Evaluating the Impact of Different Factors on Voxel-Based Classification Methods of ADNI Structural MRI Brain Images. International Journal of Biomedical Data Mining.2011;.
138. Amanda Pennington, et al.  Direct Actions of Granulocyte-Colony Stimulating Factor on Human Neuronal and Monocytic Cell Lines. J Alzheimers Dis Parkinsonism. 2013; 3: 121.
139. Lucy Elisabeth James and Ayodeji A Asuni , et al.  Parkinson’s Disease and the “Sunshine” Vitamin. J Alzheimers Dis Parkinsonism. 2013; 3: 120.
140. Khanh vinh quoc Lng and Lan Thi Hoang Nguyen , et al.  Environmental Factors in Alzheimer’s and Parkinson’s Diseases. J Alzheimers Dis Parkinsonism. 2013; 3: 119.
141. Yasumasa Ohyagi and Katsue Miyoshi , et al.  Aluminum and Alzheimer’s Disease: An Update. J Alzheimers Dis Parkinsonism. 2013; 3: 118.
142. Temporo-Parietal Brain Network Impairment Is Related To EEG ALPHA3/ALPHA2 Power Ration in Prodormal Alzheimer’s Disease. J Neurol Neurophysiol 2013, et al...;.
143. Christiane Reitz and Giuseppe Tosto , et al.  Inflammation, Immune System and Alzheimer’s disease: A Review of the Findings from the Major GWAS Studies. J Mol Genet Med. 2013; 7: 60.
144. Exposure of Engineered Nanomaterials and Its Potential Contribution to Alzheimer\'s Pathophysiology. Biochem & Pharmacol 2013.
145. Yuri L Lyubchenko , et al.  Nanoimaging for Molecular Pharmaceutics of Alzheimer’s and other Neurodegenerative Disorders. J Mol Pharm Org Process Res. 2013; 1: e107.
146. Ivan Carrera and Ramon Cacabelos, et al.  Novel Immunotherapeutic Procedures for Prevention of Alzheimer\'s Disease. Drug Des. 2013; 2: 107.
147. Haigang Gu , et al.  Modeling and Therapeutic Strategies of Pluripotent Stem Cells for Alzheimer’s Disease.  J Stem Cell Res Ther. 2013; 3: e115.
148. Jennifer Madeo and Chris Elsayad , et al.  The Role of Oxidative Stress in Alzheimer’s Disease. J Alzheimers Dis Parkinsonism. 2013; 3: 116.
149. Ayden Jacob and Sharon Cohen , et al.  A Biomedical Imaging Analysis of the Prevalent Neuropsychiatric Disorders. J Alzheimers Dis Parkinsonism. 2013; 3: 117.
150. Ayden Jacob, et al.  Abnormal Brain Circuitry and Neurophysiology Demonstrated by Molecular Imaging Modalities in Schizophrenia. J Alzheimers Dis Parkinsonism. 2013; 3: 114.
151. Fernando Pires Hartwig , et al.  Neural Cancer Stem Cells: Focusing on Chromosome Ends. J Alzheimers Dis Parkinsonism. 2013; 3: 115.
152. Dana Cristina Bodnar, et al.  Dentoperiodontal pathology in patients with Alzheimer disease. Oral Health Dent Manag. 2006;.
153. Arturo Sols Herrera, et al.  Human Photosynthesis: A Turning Point in the Understanding and Treatment of Alzheimer's Disease. J Bioanal Biomed. 2013; 5: 057.
154. Holly M Brothers, et al.  Time-Dependent Compensatory Responses to Chronic Neuroinflammation in Hippocampus and Brainstem: The Potential Role of Glutamate Neurotransmission. J Alzheimers Dis Parkinsonism. 2013; 3: 110.
155. ShihWei Lai, et al.  No Association between Chronic Osteomyelitis and Parkinson’s Disease in Older People in Taiwan. J Alzheimers Dis Parkinsonism. 2013; 3: 112.
156. Corinna M Bauer, et al.  Differentiating between Normal Aging, Mild Cognitive Impairment, and Alzheimer’s disease with FDG-PET: Effects of Normalization Region and Partial Volume Correction Method. J Alzheimers Dis Parkinsonism. 2013; 3: 113.
157. Allan Vann , et al.  Alzheimer’s Behaviors or Coincidences?. J Alzheimers Dis Parkinsonism. 2013; 3: 111.
158. David L Cross and Michael B Cross , et al.  A Clinical Analysis of Alzheimer?s Research in Neuromuscular Physical Medicine and Rehabilitation.  Int J Phys Med Rehabil. 2013; 1: 116.
159. Daniela Giacomazza and Marta Di Carlo , et al.  Insulin Resistance: A Bridge between T2DM and Alzheimer’s Disease. J Diabetes Metab. 2013; 4: 263.
160. Hadas Skaat and Shlomo Margel , et al.  Newly Designed Magnetic and Non-Magnetic Nanoparticles for Potential Diagnostics and Therapy of Alzheimer’s Disease. J Biotechnol Biomater. 2013; 3: 156.
161. Jiaqi Yao and Ahmed N. Khan , et al.  Involvement of Actin Pathology in Alzheimer’s Disease. Cell Dev Biol. 2013; 2: e121.
162. Rosie E Curiel, et al.  A New Scale for the Evaluation of Proactive and Retroactive Interference in Mild Cognitive Impairment and Early Alzheimer’s Disease. Aging Sci. 2013;.
163. Kuladip Jana, et al.  Caspases: A Potential Therapeutic Targets in the Treatment of Alzheimer’s Disease. Transl Med. 2013; S2-006.
164. John K. Grandy , et al.  Melatonin: Therapeutic Intervention in Mild Cognitive Impairment and Alzheimer Disease. J Neurol Neurophysiol. 2013; 4: 148.
165. Eric J Downer , et al.  Toll-Like Receptor Signaling in Alzheimer’s Disease Progression. J Alzheimers Dis Parkinsonism. 2013; S10-006.
166. Gardener S, et al.  Dietary Patterns Associated with Alzheimer’s Disease and Related Chronic Disease Risk: A Review. J Alzheimers Dis Parkinsonism. 2013; S10-005.
167. Aaron Carman, et al.  Chaperone-dependent Neurodegeneration: A Molecular Perspective on Therapeutic Intervention. J Alzheimers Dis Parkinsonism. 2013; S10-007.
168. Giulio Sancini, et al.  Functionalization with TAT-Peptide Enhances Blood-Brain Barrier Crossing In vitro of Nanoliposomes Carrying a Curcumin-Derivative to Bind Amyloid-Β Peptide. J Nanomed Nanotechnol. 2013; 4: 171.
169. Xiao Li and Can Zhang , et al.  Amyloidopathy in the Eye of Alzheimer′s Disease. J Addict Res Ther. 2013; S5: 005.
170. Paul J Tuite, et al.  Magnetic Resonance Imaging. 2013.
171. Alzheimer’s Disease and the Conflict between Ethics.
172. Boris DeCourt, et al.  Recent Perspectives on APP, Secretases, Endosomal Pathways and How they Influence Alzheimer\'s Related Pathological Changes in Down Syndrome. J Alzheimers Dis Parkinsonism. 2013; S7-002.
173. Ronan OCaoimh, et al.  Screening for Alzheimer\'s Disease in Downs Syndrome. J Alzheimers Dis Parkinsonism. 2013; S7-001.
174. Gjumrakch Aliev, et al.  Mitochondria Specific Antioxidants and their Derivatives in the Context of the Drug Development for Neurodegeneration and Cancer. Drug Des. 2013; 2: 103.
175. ShiBin Cheng , et al.  Herpes Simplex Virus Linked to Alzheimer’s Disease. J Trop Dis. 2013; 1: e103.
176. Mitchell Clionsky and Emily Clionsky , et al.  The Memory Orientation Screening Test..2013;.
177. Soraya L Valles , et al.  Is it Normal to have Alzheimer and Cancer at the Same Time?. Anaplastology. 2013; 2: 105.
178. Sebastiaan Engelborghs , et al.  CSF Biomarkers for Alzheimer Disease Diagnosis: Recent and Future Perspectives. J Neurol Disord. 2013; 1: e102.
179. Danielle Meola, et al.  Loss of Neuronal Phenotype and neurodegeneration: Effects of T Lymphocytes and Brain Interleukin-2. J Alzheimers Dis Parkinsonism. 2013; S10-003.
180. Federico Bilotta, et al.  Insulin Signaling in the Central Nervous System and Alzheimer’s Disease. J Alzheimers Dis Parkinsonism. 2013; 3: e129.
181. Eef Hogervorst and Angela Clifford , et al.  What is the Relationship between Higher Levels of Education Delaying Age at Onset of Dementia?. J Alzheimers Dis Parkinsonism. 2013; 3: e128.
182. Yaqiong Niu, et al.  Neuronal Cell Cycle Regulation of Cdk5 in Alzheimer’s Disease. Brain Disord Ther. 2013; S1-004.
183. Richard J. Kryscio and Erin L. Abner , et al.  Are Markov and semi-Markov Models Flexible Enough for Cognitive Panel Data?. J Biom Biostat. 2013; 4: e122.
184. Kayla C. Castellani, et al.  Treating Alzheimer Disease: Is Diet and Exercise more Effective than Small Molecule Therapy?. J Membra Sci Technol.2013; 3: e111.
185. Soraya L Valles , et al.  Astrocytes and the Important Role in the Future Research of Brain. J Alzheimers Dis Parkinsonism. 2012; 2: e127.
186. Perry EA, et al.  Failure of Aβ Removal to Improve Alzheimer’s Dementia Opens the Door to New Thinking. J Alzheimers Dis Parkinsonism. 2012; 2: e126.
187. Luigi Iuliano, et al.  Antioxidants and Cognitive Function: Misleading Concepts and New Strategies. J Alzheimers Dis Parkinsonism. 2012; 2: e125.
188. Missing Data Methods for Partial Correlations. J Biom Biostat 2012, et al...;.
189. Haigang Gu and Dahong Long , et al.  Application of Nerve Growth Factor in Alzheimer’s Disease. Clin Pharmacol Biopharm. 2012; 1: e109.
190. Garth F Hall , et al.  Is it Premature to assume that Prion-like Propagation of Protein Misfolding is the Universal Model of Lesion Spread in Neurodegeneration?. J Alzheimers Dis Parkinsonism. 2012; 2: e124.
191. Valerie L Reeves and M Paul Murphy , et al.  Assessment of Inflammation as an Alzheimer’s Disease Predictor. J Alzheimers Dis Parkinsonism. 2012; 2: e123.
192. Yasumasa Ohyagi , et al.  Apomorphine: A Novel Efficacy for Alzheimer’s Disease and Its Mechanisms. J Alzheimers Dis Parkinsonism. 2012; 2: e122.
193. Daniela Giacomazza and Marta Di Carlo , et al.  Insulin as Therapeutic Agent against Alzheimer’s Disease. Drug Des. 2013; 2: e112.
194. Jack C de la Torre , et al.  A Tipping Point for Alzheimer’s Disease Research. J Alzheimers Dis Parkinsonism. 2012; 2: e120.
195. GSK-3β, Adult Neurogenesis and Neurodegeneration. J Alzheimers Dis Parkinsonism. 2012.
196. Roxana O Carare and Cheryl Hawkes , et al.  Alzheimer’s Disease: A Failure of Clearance of Soluble Metabolites from the Ageing Brain. J Addict Res Ther. 2013; S5: e001.
197. Giuseppe Sancesario, et al.  Increased Detection of Aβ Oligomers in the Cerebrospinal Fluid of Alzheimer s Disease: Fact or Artifact?. J Mol Biomark Diagn. 2012; 3: e107.