The phospho-tau cascade, basal forebrain neurodegeneration, and dementia in Alzheimer's disease: Anti-neurodegenerative benefits of acetylcholinesterase inhibitors

 Your competent? doctor needs to know everything about this because of your likely chance of dementia post stroke.  Is your doctor competent enough to prevent your dementia?  Better ask them now before you need it.

Of course your competent? doctor knew about this earlier research: There is growing evidence that Alzheimer’s disease drugs called acetylcholinesterase inhibitors (including Aricept, Exelon and Razadyne) can improve aphasia in stroke patients.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

The phospho-tau cascade, basal forebrain neurodegene ration, and dementia in Alzheimer's disease: Anti-neurodegenerative benefits of acetylcholinesterase inhibitors

Donald E Moss https://orcid.org/0000-0003-2626-2511 dmoss@utep.edu and Ruth G PerezView all authors and affiliations

OnlineFirst

• • Abstract
  • Introduction
  • NGF is key to the survival of the basal forebrain, and its cholinergic phenotype, in the healthy brain and its susceptibility to impairment in AD
  • The acetylcholine-NGF trophic feedback loop in the healthy brain that is required for basal forebrain survival
  • Disruption of the acetylcholine-NGF feedback loop caused by phospho-tau interference with retrograde NGF transport
  • Anti-neurodegenerative benefits of AChE inhibitors
  • Discussion
  • Acknowledgments
  • Declaration of conflicting interests
  • Funding
  • ORCID iD
  • References
• PDF / ePub
• • Cite article
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  • Information, rights and permissions
  • Metrics and citations
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Abstract

A conundrum in Alzheimer's disease (AD) is why the long-term use of acetylcholinesterase (AChE) inhibitors, intended for treatment of dementia, results in slowing neurodegeneration in the cholinergic basal forebrain, hippocampus, and cortex. The phospho-tau cascade hypothesis presented here attempts to answer that question by unifying three hallmark features of AD into a specific sequence of events. It is proposed that the hyperphosphorylation of tau protein leads to the AD-associated deficit of nerve growth factor (NGF), then to atrophy of the cholinergic basal forebrain and dementia. Because the release of pro-nerve growth factor (pro-NGF) is activity-dependent and is controlled by basal forebrain projections to the hippocampus and cortex, our hypothesis is that AChE inhibitors act by increasing acetylcholine-dependent pro-NGF release and, thus, augmenting the availability of mature NGF and improving basal forebrain survival. If correct, improved central nervous system-selective AChE inhibitor therapy started prophylactically, before AD-associated basal forebrain atrophy and cognitive impairment onset, has the potential to delay not only the onset of dementia but also its rate of advancement. The phospho-tau hypothesis thus suggests that preventing hyperphosphorylation of tau protein, early should be a high priority as a strategy to help reduce dementia and its associated widespread social and economic suffering.