Alzheimer Disease: A Neurogenetic Connection

Abstract

Alzheimer Disease (AD) is a neurodegenerative issue that gradually dissolves a portion of the features of human cognizance. Amid the neurotic course of AD, beta-amyloid plaques structure which- reasons harm to neurons and results in the gross loss of cerebrum volume. As a result of AD, the harassed individual creates diminishes in intellectual/official capacity, memory impedance/misfortune, and the failure to restrain unseemly practices. Another method for saying this is that the tormented individual stops to be the individual whom they once were, i.e., their modalities of awareness has weakened. Changes in a few qualities, e.g., the quality variation APOE-epsilon4, APP, PSEN1, PSEN2, and TREM2 have all been associated with the expanded frequency and more quick movement of AD. This has offered backing to the suggestion that there are neurogenetic relates of cognizance (NgCC). In past works, these NgCC have been portrayed into three neurogenetic periods of human awareness. Promotion is an essential sample of quality based neurodegeneration that can happen in the third neurogenetic stage. There is trust that manifestations of AD may be switched with the improvement of novel hereditary treatments. Some quality treatments are in progress, e.g., FGF2, leptin, and NEU1 with the point of switching AD symptomatology. On the off chance that these quality treatments are one day fruitful in turning around a percentage of the manifestations of AD, would they be able to in the end be utilized to upgrade human cognizance in people without AD?. Amid the most recent couple of decades a huge writing has advanced, proposing that tactile brokenness, especially smell and taste brokenness, can be early markers for neurodegenerative ailments, for example, Parkinson's and Alzheimer's and neuropsychiatric infections including ADHD and Schizophrenia, all illnesses that include dopaminergic pathology. Smell misfortune and taste brokenness show up in clinical versus non-clinical gatherings, and in longitudinal studies these side effects have been noted years sooner than engine signs in the first degree relatives of people who as of now have the illnesses.

Keywords

Alzheimer disease; Human consciousness; Neurogenetic connection

Introduction

In a few scholastic fields, e.g., theory, brain research, and neuroscience- humanity has grappled with the idea of cognizance. Characterizing cognizance can be troublesome in light of the fact that it is mulled over by various fields and there is no onesided assention in all cases on the most proficient method to characterize it. The trouble characterizing awareness has been examined in different works that have been referenced for further request [1-3]. I will, however quickly, show just a couple of the different perspectives of cognizance. Panpsychism is for the most part characterized as perspective in which all things have mind or what one would consider a see any problems like quality. This idea reaches out back to the antiquated presocratic Greek logicians, e.g., Heraclitus [4-8]. Along these lines it must be contemplated that the old Greeks did not have a word for cognizance as such. Consequently, psyche or brain like quality would be synonymous with what most cutting edge neurologists and cognizance analysts would allude to as awareness. Also, relating to the meaning of panpsychism, things regularly alludes to frameworks or accumulations of frameworks, e.g., cells or creatures. So in the panpsychist see all things in the universe have a level of awareness.

There are some awareness analysts who consider cognizance (called c-substrate) to be a component of the universe equivalent (and fastened) to space and time. This idea was initially characterized by neuropsychiatrist Vernon Neppe and physicist Edward Close in their triadic dimensional vortical paradigm (TDVP) in where space-time-cognizance are fastened from the source purpose of the universe and reach out through numerical measurements [9-15].

The perspectives of panpyschism and the TVDP may vary from what a scholar, a therapist, or a neurobiologist may consider awareness while typifying a human model. Case in point, a thinker whom is a supporter of dualism may see the brain and mind as two different elements. In this way, as per a dualist, psyche is not the same as cerebrum in light of the fact that this logic keeps up that there is a mental non-material world and a physical material world, i.e., there is dualism [15-17].

At this point, an essential and thorough meaning of human awareness could be- an aggregate totality of mindfulness, substantial (or physical) sensations, discernments (tangible information and neurobiological data), feelings, contemplations, and memories of the self-inside of a minute on the time continuum [1]. On the other hand, as beforehand specified, there are a sundry of different meanings of cognizance, which have been quickly talked about in the presentation, however now give us a chance to concentrate on a neurobiological meaning of human awareness [17-21].

A general neurobiological meaning of human cognizance proposes three essential ideas: 1) awareness develops essentially from a comprehension of neuronal action 2) cognizance is not a discrete operation of the cerebrum, yet rather, the result of computational movement of the related regions of the mind 3) cognizance is a discrete marvel and that the issues of subjectivity, solidarity, and deliberateness must be stood up to in the event that we are to see how our experience is built [8].

Another closely resembling methodology, known as the neural associates of cognizance (NCC), was proposed by Francis Crick and Christopher Koch in 1990. By definition, NCC are the insignificant neuronal components together adequate for any one particular cognizant guideline or occasion [22-27]. It can be seen inside of this recommendation that mind frameworks are dynamic in pair with the cognizant experience. What's more, NCC can exhibit that there are subjective contrasts between the neural movement connected with the cognizant and oblivious psychological procedure [26-30].

The brain is the focal point of the sensory system and an essential piece of the body going about as a noteworthy managing and passing on organ to keep up the body's homeostasis because of changes in both the outside and inward environment. Mind comprises of pretty nearly 100 billion neurons and 1 trillion glial cells [1]. The association between two neurons is known as neurotransmitter, which is in charge of stream of data as minor substance heartbeats discharged by one neuron and taken up by the meeting neuron. Distinctive sorts and qualities of signs move continually through the mind's signals, making the cell premise of recollections, contemplations, and abilities [28-34].

In a late study, using high-density electroencephalography (HD-EEG) signals that can be dissected by a novel record called the perturbational complexity Index (PCI) has been tried on the human mind [12]. This strategy empowers specialists to watch what happens to the mind electronically when it is reacting to jolt. This new EEG-inferred record of human cognizance gives preparatory verification of electric relates of awareness. Furthermore, this new procedure could turn into a straightforward noninvasive estimation to recognize cognizant and oblivious states, for instance: 1) in patients with mind harm who presentation fluctuating levels of awareness 2) insignificantly cognizant state 3) lock-in disorder -a condition in where the patient is cognizant however can't move or talk [35-38].

What has been made clear with the revelation of NCC and comparing studies with PET, fMRI, and now with HD-EEG is that human cognizance can be seen on a neurophysiologic field. Scientists now have a multimodal way to deal with watch what districts of the cerebrum are invigorated amid the cognizant experience and how network between mind locales is essential. Then again, what is underneath this luxurious maze of cerebrum districts and interconnecting neurons? The answer is DNA. Give us a chance to now take a gander at a neurogenetic record of human awareness [39-45].

Neuropsychological evaluations that test consideration compass, memory, dialect aptitudes, thinking, arranging, association abilities, and even the capacity to self-reference on long haul rambling memory have shown ailment movement related decrease in AD patients [19,20]. Indeed, even a basic test that can make a gross evaluation of cognizance, e.g., the Glasgow Coma Scale, has exhibited that in AD patients there are reductions in the capacity to react to verbal order or difficult boosts, disabilities in evoking a verbal reaction, and debilitations in engine reactions [46-54].

Amid the progression of AD dynamic debilitation of day by day living results and in the last stages patients can get to be quiet, incontinent, and confined to bed. At the later phase of AD the patient is totally dependent on a parental figure for even the most fundamental needs. Basically, the AD tolerant slowly misfortunes subjective practicality as modalities of human cognizance are reduced. In the long run, they stop to be the individual that they once were [54-59]. At long last, a standout amongst the most decimating parts of AD is that while the patient proceeds with the dynamic way of reduction of mental action, the friends and family and relatives must lay witness to this disastrous move. The signs and side effects of AD are specifically identified with the fundamental pathophysiology which is fundamentally the amassing in beta-amyloid plaques and the vicinity of neurofibrillary tangles that are made out of helical hyperphosphorylated tau protein. Areas of the mind connected with awareness additionally show changes amid the movement of AD. From a neurological angle, certain modalities of human cognizance are dependent on the capacity of different mind districts, e.g., the cerebrum stem, basal forebrain, and diencephalic ranges (thalamus and hypothalamus)- all of which bolster general excitement [22-26].

Neurophysiologic anomalies have been shown in these mind locales in patients with AD [27-29]. Besides, the working of the thalamocortical systems is vital for the human cerebrum to wind up mindful of, furthermore to react to, jolts from both the outside and inner situations [22,30-33]. These locales have shown anomalies in capacity and network in patients with AD [34,35]. Regarding human cognizance, the greater part of the signs and indications of AD are an interminable strike on numerous modalities of human awareness. Case in point, this can be seen most significantly when one is no more ready and orientated times three (AOX3), loses the capacity to process and store new data, loses the capacity to segregate the earth (recognize what items are and their essentialness), exhibits diminishes in excitement/mindfulness, and the improvement of mind flights and silly thinking [55-60]. Fantasies and whimsical speculation are imperative elements on the grounds that they speak to the breakdown in the view of reality- an unsettling influence in the continuum of human cognizance [61-68].

It is extremely significant that there is a neurogenetic association in the middle of AD and human cognizance on the grounds that now hereditary anomalies can be connected with interruptions and reductions in the continuum of human awareness [69-75]. As of now there are a few quality competitors that assume a discernable part in the neurogenetics of human cognizance. Since there is a hereditary connection to disarranges like AD, it would bode well that hereditary treatments may hold the keys to a cure. Right now there are no medicines that are illness altering operators or that can invert the pathophysiology of AD. The majority of the standard medications simply decelerate the movement of the illness for a brief time of time [76-81]. These medicines give, best case scenario, minor symptomatic advantages. Inexorably, a limit is met when the aggregations of beta-amyloid and hyperphosphorylated tau protein dispense enough neuronal harm that it in the end brings about gross cerebrum misfortune. This is the final aftereffect of AD and it is irreversible [82-88].

Discussion

Right now there are no medicines that are infection altering specialists or that can switch the pathophysiology of AD. A large portion of the standard medications only decelerate the movement of the infection for a brief time of time. These medicines give, best case scenario, negligible symptomatic advantages [89-96]. Inescapably, an edge is met when the collections of beta-amyloid and hyperphosphorylated tau protein cause enough neuronal harm that it in the end brings about gross cerebrum misfortune. This is the deciding aftereffect of AD and it is irreversible. On the other hand, there may be some trust in hereditary based therapeutics [97-107]. I will quickly say three hereditary treatments went for switching a percentage of the side effects of AD:

• FGF2 transplant treatment to enhance memory in AD [108-116]. In this study FGF2 quality was exchanged specifically to the hippocampus of bigenic mice (APP+presenilin-1). The FGF2 quality was conveyed by an adeno-related infection serotype 2/1 mixture. Huge change was found in the mice getting the infusion at both the preand post-symptomatic phases of Alzheimer sickness. This was checked by testing spatial adapting in the outspread arm water maze test.

• NEU1 Gene Therapy [117-125]. This study exhibited that insufficiencies of the lysosomal sialidase, which is created by the NEU1 quality, prompts the unconstrained event of an Alzheimer-like amyloidogenic procedure to happen in the brains of mice. Also, this study along these lines exhibited that cerebral infusion of NEU1 in Alzheimer-mice brought about significant diminishment of beta-amyloid plaques. This gives it potential to really switch one of the fundamental pathologies of AD [125-130].

• Leptin gene therapy [131]. This study exhibited that leptin gene therapy had the capacity lessen the aggregation of betaamyloid in the APP/PS1 transgenic mouse model. In this study, a lentivirus vector communicating leptin protein in a self-enacting HIV-1 was conveyed by intra-cerebroventricular organization. This brought about a lessening of beta-amyloid aggregation and a halfway save of synaptic thickness in these mice [132-140].

Prior it was talked about that there is a huge association between certain quality transformations and a relationship to AD [141-145]. In this segment it can be seen that there is likewise a huge association between quality treatment and the likelihood of curing AD and protecting capacity, e.g., memory, or conceivably turning around the fundamental pathophysiology [145-149]. In the event that quality treatments can restore modalities of human awareness that were once taken away by AD pathophysiology, then this braces the neurogenetic association with human cognizance. Another method for taking a gander at this would be that, first there are sure quality changes can diminish modalities of human cognizance as found in AD and examined in this paper. Also, there are a few potential hereditary treatments that may safeguard or restore those modalities of awareness. This is the neurogenetic association [150].

At this point we must stop and ask ourselves, if hereditary treatments, for example, the ones quickly examined in this paper, were to some time or another be effective, would they be able to thusly be utilized on people without AD for purpose of human improvement? This is an imperative theme to introduce as it summons numerous moral inquiries; e.g., ought to neurogenetic improvement be lawful, what amount of upgrade ought to be permitted in people, and who will have entry to these sorts of treatments? In prior distributions the point of hereditary improvements and the issues that could perhaps follow have been talked about. Notwithstanding the likelihood of developing human cognizance, neurogenetic treatments could prompt transhumanism, or perchance, posthumanism [151,152].

Conclusion

A brief overview of various perspectives of cognizance and the neurobiological way to deal with human awareness was talked about. A few cases of NCC were outlined. It was brought up that underneath this arrangement of cerebrum districts and neurons running in pair with the cognizant experience lives a shrouded domain of NgCC. The three neurogenetic periods of awareness were quickly sketched out. It is in the third neurogenetic stage in where AD serves as an astounding illustration to outline the negative impacts of neurodegeneration on the degrees of human cognizance. This is principally in light of the fact that there are hereditary connects that have been distinguished, and more are being explored, that can be connected with the breakdown of intellectual capacities and modalities of awareness amid the decrease in the continuum of human cognizance. It has been exhibited in this work that a neurodegenerative malady, e.g., AD can reveal insight into the comprehension of human awareness.

Considerably more critical is that it gives the idea that the cure for AD appears to suggest upgrade with hereditary treatments, which if effective will invigorate the proposition of a neurogenetic association with human cognizance. At last, it should likewise be taken under thought that hereditary treatments being created to cure AD or to invert the basic pathophysiology, if one day fruitful, could likewise be utilized for human improvement conceivably opening the entryways to transhumanism, and possibly, posthumanism. This plausibility has to a great extent been disregarded and desperately needs to be talked about.

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. AguirreRueda D, et al. Pro-Oxidant and Inflammatory Mediators Produced In Transgenic Mice.
3. 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.
4. 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.
5. 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.
6. 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.
7. SIRT1 Protects Dendrites, et al...;.
8. BradleyWhitman MA and Lovell MA , et al. Increased Oxidative Damage in RNA in Alzheimer’s Disease Progression. J Anal Bioanal Tech. 2014; S2:004.
9. Gabriela Beatriz Acosta , et al. In Search of the Mysterious Alzheimer’s Disease. Clin Exp Pharmacol. 2012; S6:001.
10. Sachiko Yokoyama, et al. Escitalopram for Delusion in an Oldest Old Patient with Alzheimer’s Disease. Brain Disord Ther. 2013; 2:108.
11. Mohit Jain, et al. Data Adaptive Rule-based Classification System for Alzheimer Classification. J Comput Sci Syst Biol. 2013; 6:291-297.
12. 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.
13. Koji Hori, et al. Mini Review: Pharmacotherapy for Behavioral and Psychological Symptoms in Alzheimer?s Disease. Brain Disord Ther. 2013; 2:106.
14. 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.
15. Jun Iwamoto and Yoshihiro Sato , et al. Strategy for Prevention of Hip Fractures in Patients with Alzheimer's Disease. General Med. 2013; 1:114.
16. 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.
17. 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.
18. 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;.
19. 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.
20. Lucy Elisabeth James and Ayodeji A Asuni , et al. Parkinson’s Disease and the “Sunshine” Vitamin. J Alzheimers Dis Parkinsonism. 2013; 3:120.
21. 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.
22. Yasumasa Ohyagi and Katsue Miyoshi , et al. Aluminum and Alzheimer’s Disease: An Update. J Alzheimers Dis Parkinsonism. 2013; 3:118.
23. Temporo-Parietal Brain Network Impairment Is Related To EEG ALPHA3/ALPHA2 Power Ration in Prodormal Alzheimer’s Disease. J Neurol Neurophysiol 2013, et al...;.
24. 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.
25. Exposure of Engineered Nanomaterials and Its Potential Contribution to Alzheimer\'s Pathophysiology. Biochem & Pharmacol 2013.
26. 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.
27. Ivan Carrera and Ramon Cacabelos, et al. Novel Immunotherapeutic Procedures for Prevention of Alzheimer\'s Disease. Drug Des. 2013; 2:107.
28. Haigang Gu , et al. Modeling and Therapeutic Strategies of Pluripotent Stem Cells for Alzheimer’s Disease. J Stem Cell Res Ther. 2013; 3:e115.
29. Jennifer Madeo and Chris Elsayad , et al. The Role of Oxidative Stress in Alzheimer’s Disease. J Alzheimers Dis Parkinsonism. 2013; 3:116.
30. Ayden Jacob and Sharon Cohen , et al. A Biomedical Imaging Analysis of the Prevalent Neuropsychiatric Disorders. J Alzheimers Dis Parkinsonism. 2013; 3:117.
31. Ayden Jacob, et al. Abnormal Brain Circuitry and Neurophysiology Demonstrated by Molecular Imaging Modalities in Schizophrenia. J Alzheimers Dis Parkinsonism. 2013; 3:114.
32. Fernando Pires Hartwig , et al. Neural Cancer Stem Cells: Focusing on Chromosome Ends. J Alzheimers Dis Parkinsonism. 2013; 3:115.
33. Dana Cristina Bodnar, et al. Dentoperiodontal pathology in patients with Alzheimer disease. Oral Health Dent Manag. 2006;.
34. 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.
35. 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.
36. 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.
37. 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.
38. Allan Vann , et al. Alzheimer’s Behaviors or Coincidences?. J Alzheimers Dis Parkinsonism. 2013; 3:111.
39. 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.
40. Daniela Giacomazza and Marta Di Carlo , et al. Insulin Resistance: A Bridge between T2DM and Alzheimer’s Disease. J Diabetes Metab. 2013; 4:263.
41. 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.
42. Jiaqi Yao and Ahmed N. Khan , et al. Involvement of Actin Pathology in Alzheimer’s Disease. Cell Dev Biol. 2013; 2:e121.
43. 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;.
44. Kuladip Jana, et al. Caspases: A Potential Therapeutic Targets in the Treatment of Alzheimer’s Disease. Transl Med. 2013; S2-006.
45. John K. Grandy , et al. Melatonin: Therapeutic Intervention in Mild Cognitive Impairment and Alzheimer Disease. J Neurol Neurophysiol. 2013; 4:148.
46. Eric J Downer , et al. Toll-Like Receptor Signaling in Alzheimer’s Disease Progression. J Alzheimers Dis Parkinsonism. 2013; S10-006.
47. 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.
48. Aaron Carman, et al. Chaperone-dependent Neurodegeneration: A Molecular Perspective on Therapeutic Intervention. J Alzheimers Dis Parkinsonism. 2013; S10-007.
49. Giulio Sancini, et al. Functionalization with TAT-Peptide Enhances Blood-Brain Barrier Crossing In vitro of Nanoliposomes Carrying a Curcumin-Derivative to Bind Amyloid-? Peptide. J Nanomed Nanotechnol. 2013; 4:171.
50. Xiao Li and Can Zhang , et al. Amyloidopathy in the Eye of Alzheimer's Disease. J Addict Res Ther. 2013; S5:005.
51. Paul J Tuite, et al. Magnetic Resonance Imaging. 2013.
52. Alzheimer’s Disease and the Conflict between Ethics.
53. 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.
54. Ronan OCaoimh, et al. Screening for Alzheimer\'s Disease in Downs Syndrome. J Alzheimers Dis Parkinsonism. 2013; S7-001.
55. 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.
56. ShiBin Cheng , et al. Herpes Simplex Virus Linked to Alzheimer’s Disease. J Trop Dis. 2013; 1:e103.
57. Mitchell Clionsky and Emily Clionsky , et al. The Memory Orientation Screening Test..2013;.
58. Soraya L Valles , et al. Is it Normal to have Alzheimer and Cancer at the Same Time?. Anaplastology. 2013; 2:105.
59. Sebastiaan Engelborghs , et al. CSF Biomarkers for Alzheimer Disease Diagnosis: Recent and Future Perspectives. J Neurol Disord. 2013; 1:e102.
60. 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.
61. Federico Bilotta, et al. Insulin Signaling in the Central Nervous System and Alzheimer’s Disease. J Alzheimers Dis Parkinsonism. 2013; 3:e129.
62. 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.
63. Yaqiong Niu, et al. Neuronal Cell Cycle Regulation of Cdk5 in Alzheimer’s Disease. Brain Disord Ther. 2013; S1-004.
64. 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.
65. 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.
66. Soraya L Valles , et al. Astrocytes and the Important Role in the Future Research of Brain. J Alzheimers Dis Parkinsonism. 2012; 2:e127.
67. Perry EA, et al. Failure of Aß Removal to Improve Alzheimer’s Dementia Opens the Door to New Thinking. J Alzheimers Dis Parkinsonism. 2012; 2:e126.
68. Luigi Iuliano, et al. Antioxidants and Cognitive Function: Misleading Concepts and New Strategies. J Alzheimers Dis Parkinsonism. 2012; 2:e125.
69. Missing Data Methods for Partial Correlations. J Biom Biostat 2012, et al...;.
70. Haigang Gu and Dahong Long , et al. Application of Nerve Growth Factor in Alzheimer’s Disease. Clin Pharmacol Biopharm. 2012; 1:e109.
71. 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.
72. 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.
73. Yasumasa Ohyagi , et al. Apomorphine: A Novel Efficacy for Alzheimer’s Disease and Its Mechanisms. J Alzheimers Dis Parkinsonism. 2012; 2:e122.
74. Daniela Giacomazza and Marta Di Carlo , et al. Insulin as Therapeutic Agent against Alzheimer’s Disease. Drug Des. 2013; 2:e112.
75. Jack C de la Torre , et al. A Tipping Point for Alzheimer’s Disease Research. J Alzheimers Dis Parkinsonism. 2012; 2:e120.
76. GSK-3ß, Adult Neurogenesis and Neurodegeneration. J Alzheimers Dis Parkinsonism. 2012.
77. 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.
78. Giuseppe Sancesario, et al. Increased Detection of Aß Oligomers in the Cerebrospinal Fluid of Alzheimer s Disease: Fact or Artifact?. J Mol Biomark Diagn. 2012; 3:e107.
79. 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.
80. 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.
81. 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.
82. Reiber H, et al. Neurochemical Dementia Diagnostics – Interlaboratory Variation of Analysis, Reference Ranges and Interpretations J Alzheimers Dis Parkinsonism.2014; 4:147.
83. Shin HW, et al. Differences in BDNF Serum Levels in Patients with Alzheimer’s Disease and Mild Cognitive Impairment J Psychiatry.2015; 18: 245
84. Pasha EP, et al. Ethnoracial Disparities in Alzheimer’s Disease: Target on Cardiovascular Risks via Lifestyle Changes? J Gerontol Geriat Res.2014; 3:128.
85. Ressner P, et al. Computer-Assisted Cognitive Rehabilitation in Stroke and Alzheimer’s disease J Neurol Neurophysiol.2014; 5:260.
86. 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.
87. 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.
88. Hanby MF, et al. Emotional and Cognitive Processing Deficits in People with Parkinson ’s Disease and Apathy J Alzheimers Dis Parkinsonism.2014; 4:156.
89. 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.
90. Davey DA , et al. Alzheimer’s Disease, Cerebrovascular Disease and Dementia: A Potentially Preventable and Modifiable Syndrome J Alzheimers Dis Parkinsonism.2015; 5:184.
91. 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.
92. 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.
93. 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.
94. Lukiw WJ, et al. Microbial Sources of Amyloid and Relevance to Amyloidogenesis and Alzheimer’s Disease.2015;
95. Jana P, et al. Epidemiology and Genetics of Alzheimer’s Disease J Alzheimers Dis Parkinsonism.2015; 5:172.
96. Gareri P, et al. The Role of Quetiapine in the Treatment of Alzheimer's Disease J Gerontol Geriatr Res.2015; 4:197
97. 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.
98. Kim H, et al. A Voxel-Based Morphometry Study in Alzheimer’s Disease and Mild Cognitive Impairment J Psychiatry.2015; 18:237.
99. Ramdani L, et al. Multifunctional Curcumin-Nanocarriers Based on Host-Guest Interactions for Alzheimer Disease Diagnostic J Nanomed Nanotechnol.2015; 2015, 6:270
100. 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
101. 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
102. 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
103. 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
104. 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
105. Orwa Aboud and Sue T. Griffin W, et al. Silver Staining of Alzheimer's Disease J Neurol Disord.2014; 2014, 2: i103
106. Pavel Ressner, et al. Computer-Assisted Cognitive Rehabilitation in Stroke and Alzheimer’s disease J Neurol Neurophysiol,.2014; 5:260
107. Pranami Bhaumik, et al. A Rare Intronic Variation of Presenilin-1.2014; 1
108. Astrid Haram, et al. Clinical Correlates of RBD in Early Parkinson Disease J Alzheimers Dis Parkinsonism.2014; 2014, 4:174
109. 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
110. Victoria I Bunik, et al. Benefits of Thiamin.2014;
111. 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
112. Hyun Kim, et al. Differences in C-reactive Protein Level in Patients with Alzheimers Disease and Mild Cognitive Impairment J Psychiatry.2015;
113. David R. Borchelt, et al. Proteostasis and Secondary Proteinopathy in Alzheimer’s Disease J Alzheimers Dis Parkinsonism.2014; 2014, 4:145
114. 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
115. Borroni B, et al. Diagnosing Progressive Supranuclear Palsy: Role of Biological and Neuroimaging Markers J Alzheimers Dis Parkinsonism.2014; 2014, 4:168
116. Keiko Ikemoto, et al. Lectin-Positive Spherical Deposits.2014;
117. 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
118. 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
119. Paul Whitesman, et al. Preliminary Set Theory-Type Analysis of Proteins Associated With Parkinson’s Disease J Alzheimers Dis Parkinsonism.2014; 2014, 4:170
120. Raheel Mushtaq, et al. Comparison of Cognitive Symptoms in Subtypes of Alzheimer’s disease.2014;
121. Servello A, et al. Role of Cardiovascular Comorbidity and Depressive Symptoms on One-Year Clinical Progression of Alzheimer’s Disease.2014;
122. 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
123. 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
124. Travis H Turner, et al. Epidermal Growth Factor.2014;
125. Yellamma K, et al. Silk Protein, Sericin as a Cognitive Enhancer in Alzheimer’s Disease J Alzheimers Dis Parkinsonism.2014; 2014, 4:163
126. 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
127. 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
128. 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
129. 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
130. 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
131. 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
132. 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
133. Amir Nazem, et al. Alzheimer’s Disease Drug Discovery may be Misled by Wrong Animal Models J Gerontol Geriatr Res.2014; 2014, 3: e127
134. 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
135. Mi Tian, et al. Alzheimer’s Disease and Dementia, Under-Recognized Public Health Crisis in China J Gerontol Geriatr Res.2014; 2014, 3: 179
136. 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
137. Xuesong Chen, et al. Role of LDL Cholesterol and Endolysosomes in Amyloidogenesis and Alzheimer’s Disease J Neurol Neurophysiol.2014; 2014, 5:236
138. 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
139. James Oluwagbamigbe Fajemiroye, et al. Alzheimer’s Disease and Animal Models in Retrospect Med chem.2014; 2014, 4: 701
140. 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
141. Emanuela Onofri, et al. Cognitive Performance Deficits and Dysgraphia in Alzheimer’s Disease Patients J Neurol Neurophysiol.2014; 2014, 5:223
142. Aryal R, et al. Is the A-beta peptide of Alzheimer’s Disease an Antimicrobial Peptide? J Gerontol Geriatr Res.2014; 2014, 3: 165
143. Christian Barbato, et al. Alzheim.2014;
144. 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
145. 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
146. Nazem A, et al. Nanotechnology Building Blocks for Intervention with Alzheimer’s Disease Pathology: Implications in Disease Modifying Strategies J Bioanal Biomed.2014; 2014
147. Jacques Hugon, et al. Involvement of PKR in Alzheimer’s Disease J Alzheimers Dis Parkinsonism.2014; 2014, 4:154
148. 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
149. 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
150. 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
151. 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
152. Kentaro Horiuchi, et al. Rivastigimine for Relatively Younger Alzheimer’s Disease Patient Brain Disord Ther.2014 2014, 3:133