You can ask your doctor what pieces of the kitchen sink they are throwing at preventing Alzheiners/dementia before clinical stuff is proven.
Is this earlier research enough for your doctor to use?
Can An Anti-Asthma Drug Rejuvenate the Brain? montelukast January 2016
A Decades-Old Asthma Drug Has Reversed Brain Damage From Dementia in Mice - zileuton July 2018
Or is your doctor using one of these to prevent dementia?
1. The End of Alzheimer's: The First Program to Prevent and Reverse Cognitive Decline by Dale Bredesen
2. A Real Alzheimer's Prevention Program from The University of California
3. I'm a Brain Doctor, and This Is What I Do to Prevent Alzheimer's December 2018
4. Reversing the Alzheimer’s Catastrophe April 2007
The latest here:
Circular Dichroism Spectroscopy Identifies the β-Adrenoceptor Agonist Salbutamol As a Direct Inhibitor of Tau Filament Formation in Vitro
- David J Townsend* ,
- Barbora Mala ,
- Eleri Hughes ,
- Rohanah Hussain ,
- Giuliano Siligardi ,
- Nigel J. Fullwood , and
- David A. Middleton
Abstract
Potential
drug treatments for Alzheimer’s disease (AD) may be found by
identifying compounds that block the assembly of the
microtubule-associated protein tau into neurofibrillar tangles
associated with neuron destabilization and cell death. Here, a small
library of structurally diverse compounds was screened in vitro
for the ability to inhibit tau aggregation, using high-throughput
synchrotron radiation circular dichroism as a novel tool to monitor the
structural changes in the protein as it assembles into filaments. The
catecholamine epinephrine was found to be the most effective tau
aggregation inhibitor of all 88 screened compounds. Subsequently, we
tested chemically similar phenolamine drugs from the β-adrenergic
receptor agonist class, using conventional circular dichroism
spectroscopy, thioflavin T fluorescence, and transmission electron
microscopy. Two compounds, salbutamol and dobutamine, used widely in the
treatment of respiratory and cardiovascular disease, impede the
aggregation of tau in vitro. Dobutamine reduces both the rate and
yield of tau filament formation over 24 h; however, it has little
effect on the structural transition of tau into β-sheet structures over
24 h. Salbutamol also reduces the yield and rate of filament formation
and additionally inhibits tau’s structural change into β-sheet-rich
aggregates. Salbutamol has a good safety profile and a half-life that
facilitates permeation through the blood–brain barrier and could
represent an expediated approach to developing AD therapeutics. These
results provide the motivation for the in vivo evaluation of
pre-existing β-adrenergic receptor agonists as a potential therapy for
AD through the reduction of tau deposition.
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