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.

Thursday, December 16, 2021

Anxiety May Amplify Risk of Cognitive Impairment

 It is obviously your responsibility not to have any anxiety just because your doctor has nothing and knows nothing on getting you 100% recovered. And this is in cognitively unimpaired persons so I'm sure the risk is much greater in stroke survivors.

Anxiety May Amplify Risk of Cognitive Impairment

Amyloid-anxiety interaction appears additive

A computer rendering of amyloid plaques on a nerve cell.

Anxiety amplified the risk of mild cognitive impairment (MCI) in cognitively unimpaired people with elevated amyloid beta, a prospective study showed.

While amyloid deposits raised the risk of MCI independently, there was a significant additive interaction between amyloid and anxiety (joint effect HR 6.77, 95% CI 3.58-12.79), reported Yonas Geda, MD, MSc, of the Barrow Neurological Institute in Phoenix, and colleagues in Alzheimer's & Dementia. There was no similar effect with depression.

"This study has both scientific and public health importance," Geda told MedPage Today. "From a scientific standpoint, the study showed that amyloid protein deposition in a cognitively normal elderly person -- 70 years and older -- is associated with new-onset mild cognitive impairment after about 3 to 5 years. Additionally, if the person has anxiety, the risk of developing MCI is further amplified."

"When it comes to public health, we also found managing anxiety in old age with physical activity and social support may decrease a person's risk of MCI," Geda added.

"In the past, a smaller Australian study had arrived at a similar conclusion," he noted. "However, that study's sample was smaller and it begged to be replicated."

In their study, Geda and colleagues followed 1,440 cognitively unimpaired people from the population-based Mayo Clinic Study of Aging for a median of 5.5 years. Participants underwent baseline neuropsychological testing, Beck Depression Inventory-II (BDI-II) and Beck Anxiety Inventory (BAI) assessments, and neuroimaging. Cortical amyloid beta was measured by PET Pittsburgh compound B, and elevated deposition was defined as standardized uptake value ratio of 1.48 or more.

Median baseline age of participants was about 71 and 52.8% were men. Median education was 15 years and median number of medical comorbidities was two, measured by the Charlson Comorbidity Index. Overall, 73 people showed clinical anxiety (BAI scores of 10 or higher) and 79 people showed clinical depression (BDI-II scores of 13 or higher).

A total of 379 people had elevated amyloid deposits; these people were older (median age 77) and had 1 year less education and one more medical comorbidity than others.

Over the follow-up period, 206 people developed incident MCI. People with elevated amyloid had an increased risk of incident MCI, even without clinical anxiety (HR 1.85, 95% CI 1.38-2.49, P<0.0001) or depression (HR 2.04, 95% 1.52-2.74, P<0.0001).

After adjusting for sex, education, and medical comorbidity, a statistically significant additive interaction emerged between elevated amyloid and clinical anxiety with incident MCI (P=0.0310). The interaction between amyloid and clinical depression in predicting MCI risk was not significant.

An anxiety-amyloid interaction has appeared in smaller studies, but the mechanism behind it is unknown, Geda and colleagues said. Anxiety could be a very early marker of Alzheimer's disease and assessing anxiety could be an important way to identify patients at high risk of Alzheimer's before cognitive decline occurs, they noted.

"This finding has clinical implications in that the monitoring and possible management of anxiety among cognitively unimpaired community-dwelling persons with cortical amyloid-beta deposition may be warranted," the researchers observed.

The study has several limitations, including small sample sizes of subgroups. The sample came from Olmsted County, Minnesota, and largely consisted of white, relatively highly educated adults.

  • Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

The study was supported by the National Institute on Aging, National Institute of Mental Health, National Institute of Neurological Disorders and Stroke, Robert Wood Johnson Foundation, Robert H. and Clarice Smith and Abigail Van Buren Alzheimer's Disease Research Program, GHR Foundation, Mayo Foundation for Medical Education and Research, National Program of Sustainability II, Edli Foundation, and Arizona Alzheimer's Consortium.

Geda received funding from the NIH and Roche, and served on Lundbeck Advisory Board. Co-authors reported relationships with NIH, Roche, Biogen, Abbott Laboratories, Johnson and Johnson, Medtronic, Amgen, AVID Radiopharmaceuticals, Eisai, GE Healthcare, Bayer Schering Pharma, Piramal Life Sciences, Merck Research, Siemens Molecular Imaging, Eli Lilly, Lysosomal Therapeutics, Lundbeck, Department of Defense, AstraZeneca, the DIAN study, Alzheimer's Treatment and Research Institute at USC, and Genentech.

 

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