Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 30,656 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective 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.
Showing posts with label neurofibrillary tangles. Show all posts
Showing posts with label neurofibrillary tangles. Show all posts
This is so blasted simple. Contact the stroke leader who will update the stroke strategy with this request to solve for fewer entorhinal NFTs. Then you just get researchers to SOLVE THIS EXACT PROBLEM. Solve for preventing these entorhinal NFTs. You can't let researchers choose their own research, stroke will never be solved that way. We need a strategy and leaders to run that strategy to completion.
Advancing age is
typically associated with declining memory capacity and increased risk
of Alzheimer’s disease (AD). Markers of AD such as amyloid plaques (AP)
and neurofibrillary tangles (NFTs) are commonly found in the brains of
cognitively average elderly but in more limited distribution than in
those at the mild cognitive impairment and dementia stages of AD.
Cognitive SuperAgers are individuals over age 80 who show superior
memory capacity, at a level consistent with individuals 20–30 years
their junior. Using a stereological approach, the current study
quantitated the presence of AD markers in the memory-associated
entorhinal cortex (ERC) of seven SuperAgers compared with six
age-matched cognitively average normal control individuals. Amyloid
plaques and NFTs were visualized using Thioflavin-S histofluorescence,
6E10, and PHF-1 immunohistochemistry. Unbiased stereological analysis
revealed significantly more NFTs in ERC in cognitively average normal
controls compared with SuperAgers (P < 0.05) by a difference
of ~3-fold. There were no significant differences in plaque density. To
highlight relative magnitude, cases with typical amnestic dementia of
AD showed nearly 100 times more entorhinal NFTs than SuperAgers. The
results suggest that resistance to age-related neurofibrillary
degeneration in the ERC may be one factor contributing to preserved
memory in SuperAgers.
Now your doctors and stroke hospital need to initiate research that will create protocols that prevent these neurofibrillary tangles (NFTs). Or are you going to give your doctors and hospital a pass on their incompetence?
Advancing age is
typically associated with declining memory capacity and increased risk
of Alzheimer’s disease (AD). Markers of AD such as amyloid plaques (AP)
and neurofibrillary tangles (NFTs) are commonly found in the brains of
cognitively average elderly but in more limited distribution than in
those at the mild cognitive impairment and dementia stages of AD.
Cognitive SuperAgers are individuals over age 80 who show superior
memory capacity, at a level consistent with individuals 20–30 years
their junior. Using a stereological approach, the current study
quantitated the presence of AD markers in the memory-associated
entorhinal cortex (ERC) of seven SuperAgers compared with six
age-matched cognitively average normal control individuals. Amyloid
plaques and NFTs were visualized using Thioflavin-S histofluorescence,
6E10, and PHF-1 immunohistochemistry. Unbiased stereological analysis
revealed significantly more NFTs in ERC in cognitively average normal
controls compared with SuperAgers (P < 0.05) by a difference
of ~3-fold. There were no significant differences in plaque density. To
highlight relative magnitude, cases with typical amnestic dementia of
AD showed nearly 100 times more entorhinal NFTs than SuperAgers. The
results suggest that resistance to age-related neurofibrillary
degeneration in the ERC may be one factor contributing to preserved
memory in SuperAgers.
1.Department of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiologythe Sahlgrenska Academy at the University of GothenburgMölndalSweden
2.Wallenberg Centre for Molecular and Translational MedicineUniversity of GothenburgGothenburgSweden
3.King’s College London, Institute of Psychiatry, Psychology & NeuroscienceMaurice Wohl Clinical Neuroscience InstituteLondonUK
4.NIHR
Biomedical Research Centre for Mental Health & Biomedical Research
Unit for Dementia at South London & Maudsley NHS FoundationLondonUK
5.MTA-DE Cerebrovascular and Neurodegenerative Research Group, Department of NeurologyUniversity of DebrecenDebrecenHungary
6.Centre for Age-Related MedicineStavanger University HospitalStavangerNorway
7.Department of PsychiatryUniversity of Oxford. Warneford HospitalOxfordUK
8.Clinical Memory Research Unit, Department of Clinical Sciences, MalmöLund UniversityLundSweden
9.Department of Neurodegenerative DiseaseUCL Institute of NeurologyLondonUK
10.Clinical Neurochemistry LaboratorySahlgrenska University HospitalMölndalSweden
11.Department of Molecular NeuroscienceUCL Institute of NeurologyQueen SquareUK
12.UK Dementia Research Institute at UCL|LondonUK
Open Access
Research
First Online:
Abstract
Alzheimer’s
disease (AD) is pathologically characterized by the accumulation of
amyloid-β (Aβ) plaques, neurofibrillary tangles and widespread neuronal
loss in the brain. In recent years, blood biomarkers have emerged as a
realistic prospect to highlight accumulating pathology for secondary
prevention trials. Neurofilament light chain (NfL), a marker of axonal
degeneration, is robustly elevated in the blood of many neurological and
neurodegenerative conditions, including AD. A strong relationship with
cerebrospinal fluid (CSF) NfL suggests that these biomarker modalities
reflect the same pathological process. Yet, the connection between blood
NfL and brain tissue pathology has not been directly compared. In this
study, longitudinal plasma NfL from cognitively healthy controls (n = 12) and AD participants (n = 57) were quantified by the Simoa platform. On reaching post-mortem,
neuropathological assessment was performed on all participants, with
additional frozen and paraffin-embedded tissue acquired from 26
participants for further biochemical (Aβ1–42, Aβ1–40,
tau) and histological (NfL) evaluation. Plasma NfL concentrations were
significantly increased in AD and correlated with cognitive decline,
independent of age. Retrospective stratification based on Braak staging
revealed that baseline plasma NfL concentrations were associated with
higher neurofibrillary tangle pathology at post-mortem.
Longitudinal increases in plasma NfL were observed in all Braak
groupings; a significant negative association, however, was found
between plasma NfL at time point 1 and both its rate of change and
annual percentage increase. Immunohistochemical evaluation of NfL in the
medial temporal gyrus (MTG) demonstrated an inverse relationship
between Braak stages and NfL staining. Importantly, a significant
negative correlation was found between the plasma NfL measurement
closest to death and the level of NfL staining in the MTG at post-mortem.
For the first time, we demonstrate that plasma NfL associates with the
severity of neurofibrillary tangle pathology and neurodegeneration in
the post-mortem brain.
