Is there any relation between the activity of tangles and plaques ?
Whenever tangles are formed that will definitely leads to the death of cells . How beta amyloid affects the activity of cell ?
Yes, Alzheimer's disease is defined neuropathologically by the presence of both neurofibrillary tangles and amyloid plaques. How/if they are linked is an area of intense research with no unifying theme as yet.
Thank you Jakob and Ritchie .could you please tell be how beta amyloid plaques affect the brain functioning ? how free radicals and amyloid plaques are related ?
Well, strictly speaking there is no AD without both plaques and tangles, simply because they define the disease.
However, there are neurodegenerative dementias considered to be variants of AD, one such form is tangle-only dementia or the tangle-predominant form of senile dementia.
Brain Pathol. 1998 Apr;8(2):367-76.
Senile dementia with tangles (tangle predominant form of senile dementia).
Jellinger KA, Bancher C.
"Senile dementia with tangles is suggested to be a variant of Alzheimer disease occurring in the oldest-old, but its nosological position within aging disorders of the brain is still controversy."
This paper shows a link between tau hyper-phosphorylation and Ab
http://www.ncbi.nlm.nih.gov/pubmed/22156579
As described above, both tangles (hyperphosphorylated tau) and plaques (amyloid-Beta) are inherent to the disease. We reported last year that there are three subtypes of AD that can be classified based on the predominance of their tangles in particular brain regions (Murray et al, Lancet Neurology 2011; http://www.ncbi.nlm.nih.gov/pubmed/21802369). This prompted us to follow-up the study by investigating amyloid and tau burden differences across subtypes, as well as compare them to neurofibrillary tangle predominant dementia. We found neuropathologic, genetic, clinical, as well as demographic differences across the cases (Janocko et al, Acta Neuropath, 2012). I would like to echo Dimitrije statement earlier that we find amyloid and tangle pathology in the elderly that was insufficient to contribute to a dementing disorder.
http://www.ncbi.nlm.nih.gov/pubmed/22968369
See papers by Hiroshi Mori and colleagues in which they describe and model familial AD with a deletion in APP. This mutation leads to AD with oligomers but no plaques or tangles
Newly discovered protein shown to cause amyloid-beta plaques in Alzheimer's
- Download PDF Copy
Oct 2 2018
Researchers have known for many years that amyloid-beta protein slowly builds up in the brain, and form plaques that lead to neuronal cell death and eventually, Alzheimer’s disease (AD).
Now, scientists have discovered that a potassium channel called KCNB1 can trigger the formation of amyloid-beta plaques.
📷Image Credit: Juan Gaertner / Shutterstock
The results of a new study titled, Oxidation of KCNB1 channels in the human brain and in a mouse model of Alzheimer’s disease, were recently published in the journal Cell Death & Disease.
The study showed that when the brain is under stress, there is a build up of KCNB1. This protein is toxic to the brain’s nerve cells and triggers the production of amyloid-beta.
In the study, the build-up of activated KCNB1 channels was associated with levels of free radicals.
Indeed, scientists have known for a long time that during aging or in neurodegenerative disease cells produce free radicals. Free radicals are toxic molecules that can cause a reaction that results in lost electrons in important cellular components, including the channels.” Professor Federico Sesti, Study Co-author
Sesti added that KCNB1 is oxidated and accumulates in the brain.
He noted that most Alzheimer’s disease studies do not go beyond laboratory mice into humans, but this protein has also been studied in humans so the evidence is conclusive.
He went on to say that this protein did not only play a role in Alzheimer’s disease but also minor brain trauma.
The protein has been found to play a role in inflammatory changes in the brain and in this study, was shown to trigger the deposition of the amyloid beta protein plaques.
This study provides the first experimental evidence that oxidative modification of KCNB1 takes place in the aging human brain and is exacerbated in the Alzheimer’s brain. KCNB1 oxidation, cause neuroinflammation, amyloidosis, and cognitive impairment.”
Source:
Oxidation of KCNB1 channels in the human brain and in a mouse model of Alzheimer’s disease
- Badges
- Science topic
- Similar topics
- Psychology