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Journal of Neuroinfectious Diseases - Parkinson's Disease Associated with Cognitive Decline
E-ISSN: 2314-7326
P-ISSN: 2314-7334

Journal of Neuroinfectious Diseases
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  • Short Communication   
  • J Neuroinfect Dis, Vol 12(5)
  • DOI: 10.4172/2314-7326.1000334

Parkinson's Disease Associated with Cognitive Decline

Vincenza Aurelian

DOI: 10.4172/2314-7326.1000334

Abstract

Increasing events or objects that prove something hints that gangliosides act as important people who try to settle an argument in both demyelination and remyelination. Goal: The purpose of the present study was to ask lots of questions about/try to find the truth about the presence of IgM disease-fighters against GM1, GD1b and GQ1b gangliosides in the sera of in patients who suffered from Parkinson's disease in relationship with the medicine-based limits/guidelines. The present research is based on the act of asking questions and trying to find the truth about something for anti-ganglioside disease-fighters and healthy age-matched people, as usual/ commonly and regular/ healthy controls, using Enzyme-Linked Immuno-Sorbent tests/things to be tested. The patients showed/told about increased levels of the tested disease-fighters, compared to usual/ commonly and regular/ healthy controls. A relationship between IgM anti-GM1 and the level of thinking-related damage/weakness Minimental State Examination; Brought together as one Parkinson's Disease Rating Scale I was also saw/heard/became aware of. An off to the side neuroimmune response may happen in patients who suffer from Parkinson's disease especially those with thinking-related damage/weakness. Further (act of asking questions and trying to find the truth about something) is needed to establish a direct connection between that unable to be harmed response and disease how a disease works. One of the most impactful non-motor visible signs of Parkinson's disease (PD) is thinking-related damage/weakness. Thinking-related decline in PD exists as a (something that continues from one extreme to the other), with signs of sickness ranging from (usual/ commonly and regular/ healthy) thinking to mild thinking-related damage/weakness (MCI) and finally severe problems with thinking and living (PDD). MCI is related to medicine and science group of different things mixed together and its development or increase over time/series of events or things differs/changes with cases returning to usual/ commonly and regular/ healthy thinking. Opposite from what's expected, when severe problems with thinking and living happens, the decline is usually fast and made a prejudiced mental picture. The combination of Lewy and Brain disease disease/the study of disease is the most strong and healthy disease-related relate of PDD. There are no approved drugs for PD-MCI and the benefit from the only approved showing signs of sickness treatment for PDD is modest.

Keywords: Parkinson’s Disease; Gangliosides; Anti-Gm1; AntiGd1b; Cognitive decline

No Heading

Abstract

Increasing events or objects that prove something hints that gangliosides act as important people who try to settle an argument in both demyelination and remyelination. Goal: The purpose of the present study was to ask lots of questions about/try to find the truth about the presence of IgM disease-fighters against GM1, GD1b and GQ1b gangliosides in the sera of in patients who suffered from Parkinson's disease in relationship with the medicine-based limits/guidelines. The present research is based on the act of asking questions and trying to find the truth about something for anti-ganglioside disease-fighters and healthy age-matched people, as usual/ commonly and regular/ healthy controls, using Enzyme-Linked Immuno-Sorbent tests/things to be tested. The patients showed/told about increased levels of the tested disease-fighters, compared to usual/ commonly and regular/ healthy controls. A relationship between IgM anti-GM1 and the level of thinking-related damage/weakness Minimental State Examination; Brought together as one Parkinson's Disease Rating Scale I was also saw/heard/became aware of. An off to the side neuroimmune response may happen in patients who suffer from Parkinson's disease especially those with thinking-related damage/weakness. Further (act of asking questions and trying to find the truth about something) is needed to establish a direct connection between that unable to be harmed response and disease how a disease works. One of the most impactful non-motor visible signs of Parkinson's disease (PD) is thinking-related damage/weakness. Thinking-related decline in PD exists as a (something that continues from one extreme to the other), with signs of sickness ranging from (usual/ commonly and regular/ healthy) thinking to mild thinking-related damage/weakness (MCI) and finally severe problems with thinking and living (PDD). MCI is related to medicine and science group of different things mixed together and its development or increase over time/series of events or things differs/changes with cases returning to usual/ commonly and regular/ healthy thinking. Opposite from what's expected, when severe problems with thinking and living happens, the decline is usually fast and made a prejudiced mental picture. The combination of Lewy and Brain disease disease/the study of disease is the most strong and healthy disease-related relate of PDD. There are no approved drugs for PD-MCI and the benefit from the only approved showing signs of sickness treatment for PDD is modest.

Keywords

Parkinson’s Disease; Gangliosides; Anti-Gm1; AntiGd1b; Cognitive decline

Introduction

In most of patients with Parkinson's disease (PD), Lewy bodies clearly show/include the common symbol disease-related finding of the disease consisted mainly of α-synuclein, which is the principal part of Lewy bodies. more than two, but not a lot of studies have showed/told about that α-synuclein's misfolded deposits act as an insulting/swelling stimulator of microglia, which is further increased/got worse by the production of superoxide negatively-charged ions and other poisonous to nerves factors TNF-α, chemokines and autoantibodies, including anti-ganglioside disease-fighters [1].

However, according to other issues gangliosides seem to limit/hold down the disease-related group of α-synuclein [2]. Gangliosides are acid-like/harsh glycosphingolipids of plasma membranes. Their hydrophobic ceramide is inserted into the lipid double layer, while the water-loving headgroup consisting of nerve-related/brain-related sugar molecules and sialic acid is stuck out into the outside of a cell space. The molecular structure of the gangliosides enable them to behave as autoantibody targets. The identification of a disease or problem, or its cause of the patients was based on the UK Brain Bank Judging requirements for Parkinson's Disease [3].

The patients were unselected and in-a-row from our PD when you don't stay at a hospital overnight clinic, having no prior history off to the side nerve disease. The current neurophysiological act of asking questions and trying to find the truth about something left out/kept out also any off to the side nerve disease. Other when something is kept out or not included judging requirements included the presence of: sudden and short-term/chronic swelling, disease that can spread from person to persons, cancer, related to processing and using food or other extreme disease-related sicknesses/problems [4]. In case of Parkinson's disease, we know that α-synuclein is an insulting/swelling stimulant for microglia that binds specifically to GM1 ganglioside, whereas GM2, GM3 and asialo-GM1 have a weaker bound on α-synuclein. This bound stops the (extremely dangerous, abnormal heartbeat) of α-synuclein and its disease-related collection over time. It is possible that α-synuclein is recruited by GM1 to membranicraft areas in presynaptic terminals. In this big picture, disturbing or causing a small change in something of GM1/raft assiocation could cause changes in α-synuclein adding/giving to the how a disease started of PD [5].

References

  • McGeer PL, McGeer EG (2008) Glial reactions in Parkinson's disease. Mov Disord 23: 474-483.
  • Qian L, Flood PM, Hong JS (2010) Neuroinflammation is a key player in Parkinson's disease and a prime target for therapy. J Neural Transm 117: 971-979.
  • Rogers J, Mastroeni D, Leonard B, Joyce J, Grover A (2007) Neuroinflammation in Alzheimer's disease and Parkinson's disease: are microglia pathogenic in either disorder? Int Rev Neurobiol 82: 235-246.
  • Ouchi Y, Yagi S, Yokokura M, Sakamoto M (2009) Neuroinflammation in the living brain of Parkinson's disease. Parkinsonism RelatDisord 15 Suppl 3: S200-204.
  • Halliday GM, Stevens CH (2011) Glia: initiators and progressors of pathology in Parkinson's disease. Mov Disord 26: 6-17.
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