Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, June 22, 2019

Melatonin in Alzheimer’s Disease: A Latent Endogenous Regulator of Neurogenesis to Mitigate Alzheimer’s Neuropathology

Lots of other research on melatonin for stroke so your doctor can add this to your protocols. Your doctor does have rehab protocols for you, doesn't she? But this is ultimately useless with no amounts or protocols on the use of it.

Melatonin in Alzheimer’s Disease: A Latent Endogenous Regulator of Neurogenesis to Mitigate Alzheimer’s Neuropathology

  • Md. Farhad Hossain
  • Md. Sahab UddinEmail author
  • G. M. Sala Uddin
  • Dewan Md. Sumsuzzman
  • Md. Siddiqul Islam
  • George E. Barreto
  • Bijo Mathew
  • Ghulam Md AshrafEmail author
  1. 1.Department of Physical TherapyGraduate School of Inje UniversityGimhaeSouth Korea
  2. 2.Department of PharmacySoutheast UniversityDhakaBangladesh
  3. 3.Pharmakon Neuroscience Research NetworkDhakaBangladesh
  4. 4.Department of Rehabilitation ScienceGraduate School of Inje UniversityGimhaeSouth Korea
  5. 5.Departamento de Nutrición y Bioquímica, Facultad de CienciasPontificia Universidad JaverianaBogotá DCColombia
  6. 6.Instituto de Ciencias BiomédicasUniversidad Autónoma de ChileSantiagoChile
  7. 7.Division of Drug Design and Medicinal Chemistry Research Lab, Department of Pharmaceutical ChemistryAhalia School of PharmacyPalakkadIndia
  8. 8.King Fahd Medical Research CenterKing Abdulaziz UniversityJeddahSaudi Arabia
  9. 9.Department of Medical Laboratory Technology, Faculty of Applied Medical SciencesKing Abdulaziz UniversityJeddahSaudi Arabia
Article
First Online:

Abstract

Melatonin, a pineal gland synthesized neurohormone is known as a multifunctioning pleiotropic agent which has a wide range of neuroprotective role in manifold age-related neurodegenerative disorders especially Alzheimer’s diseases (AD). AD is a devastating neurodegenerative disorder and common form of dementia which is defined by abnormal and excessive accumulation of several toxic peptides including amyloid β (Aβ) plaques and neurofibrillary tangles (NFTs). The Alzheimer’s dementia relates to atrophic changes in the brain resulting in loss of memory, cognitive dysfunction, and impairments of the synapses. Aging, circadian disruption, Aβ accumulation, and tau hyperphosphorylation are the utmost risk factor regarding AD pathology. To date, there is no exact treatment against AD progression. In this regard, melatonin plays a crucial role for the inhibition of circadian disruption by controlling clock genes and also attenuates Aβ accumulation and tau hyperphosphorylation by regulating glycogen synthase kinase-3 (GSK3) and cyclin-dependent kinase-5 (CDK5) signaling pathway. In this review, we highlight the possible mechanism of AD etiology and how melatonin influences neurogenesis by attenuating circadian disruption, Aβ formation, as well as tau hyperphosphorylation. Furthermore, we also find out and summarize the neuroprotective roles of melatonin by the blockage of Aβ production, Aβ oligomerization and fibrillation, tau hyperphosphorylation, synaptic dysfunction, oxidative stress, and neuronal death during AD progression.

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