dementia

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Post-Stroke Cognitive Impairment And Dementia And Risk Factors and Prevention

Patrick Tomko

Dr. Rebecca Gottesman presented on Thursday during the Stroke Conference of 2021. She addressed the past, present, and future related to vascular dementia, mixed dementia, early stroke recovery, and precision medicine.

https://pubmed.ncbi.nlm.nih.gov/30784556/

In the past, the definition of post-stroke dementia was not necessarily uniform. She explains this is related to the term vascular dementia being sort of “tricky”. When classifying dementia you should consider, when you look, where you look, and whom you are looking at?

Many people can have dementia prior to having the stroke, this important when reviewing the prevalence rates after the stroke. Nearly 10% has dementia prior to stroke onset (1).

Dr. Gottesman highlights the need to review mixed pathologies for vascular dementia. The trajectories of onset and recovery vary between people. There can be a decline in cognition, followed by a recovery, then a further decline or an improvement. The Individual-level risk is important in post-stroke dementia.

https://www.ahajournals.org/doi/epub/10.1161/STROKEAHA.117.017319

Dr. Gottesman shared that the same stroke does not affect the person the same way (not every stroke leads to the same outcome). The individual risk profile will help individualize treatments and allow for more precision in medicine. She acknowledges that it is difficult to identify everyone who may have a stroke before they have an actual stroke. The meta-analysis from Oberlin highlights leisure activity as a potential way to reduce post-stroke dementia (2). Near the end of the presentation, Dr. Gottesman suggests we consider the following questions:

1) How do you consider aphasia and other cognitive deficits from the stroke?

2) How much time should pass after the stroke before you call it “dementia”?

3) How do you characterize dementia?

4) How do you characterize the dementia subtype?

5) How might future studies improve post-stroke cognitive outcomes?

We should consider the different prevention approaches due to the number of the different pathologies related to post-stroke dementia.

References

  1. Pendlebury ST, Rothwell PM. Incidence and prevalence of dementia associated with transient ischaemic attack and stroke: analysis of the population-based Oxford Vascular Study. The Lancet Neurology. 2019 Mar 1;18(3):248–58.
  2. Oberlin LE, Waiwood AM, Cumming TB, Marsland AL, Bernhardt J, Erickson KI. Effects of Physical Activity on Poststroke Cognitive Function: A Meta-Analysis of Randomized Controlled Trials. Stroke. 2017 Nov;48(11):3093–100.

“The views, opinions and positions expressed within this blog are those of the author(s) alone and do not represent those of the American Heart Association. The accuracy, completeness and validity of any statements made within this article are not guaranteed. We accept no liability for any errors, omissions or representations. The copyright of this content belongs to the author and any liability with regards to infringement of intellectual property rights remains with them. The Early Career Voice blog is not intended to provide medical advice or treatment. Only your healthcare provider can provide that. The American Heart Association recommends that you consult your healthcare provider regarding your personal health matters. If you think you are having a heart attack, stroke or another emergency, please call 911 immediately.”
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Alzheimer’s Disease: Prevention is the Best Treatment

Siddharth Sehgal, MD

Alzheimer’s disease (AD) is a progressive neurodegenerative condition and the most common cause of dementia. It accounts for about 60-80 % of all cases of dementia1. There are currently no curative or prevention therapies available for the disease. Medications prescribed for Alzheimer’s disease (AD) symptoms can temporarily help individuals with thinking, memory, or speaking skills and can help with some of the behavioral and personality changes associated with AD.  everal lines of evidence indicate that lifestyle habits and genetic factors play an important role in determining a person’s risk of developing AD2.

There have been a few recent disappointments with AD therapies when Biogen and Esai released negative results from a promising drug trial (3) and then Novartis, Amgen and Banner Alzheimer’s Institute announced in July their decision to not pursue further studies with a potential AD drug4. But new research presented at the Alzheimer’s Association International conference held in July at Los Angeles has provided evidence of a potential preventive strategy. Results from this study indicate that certain healthy lifestyle habits can reduce the risk of developing AD and even overcome the genetic risk in some susceptible individuals5.

During this retrospective cohort study,196 383 individuals aged at least 60 years, without evidence of cognitive impairment or dementia at baseline were followed for a median of 8 years. Risk assessment was performed using lifestyle and genetic risk scores. Lifestyle risk score was determined by a combination of smoking status, alcohol consumption, physical activity, and dietary habits. During the follow up period, a total of 1769 patients were diagnosed with new onset dementia. The incidence of dementia was noted in 1.23% of the high genetic risk group as compared to 0.63% in the low genetic risk cohort. The genetic risk was seen to be independent of the lifestyle factors.

About 68% participants followed a favorable lifestyle and 8% were noted to have an unfavorable lifestyle.

Dementia risk was seen to increase with worsening of lifestyle scores in a linear fashion. In the unfavorable lifestyle group, 1.16% persons developed dementia while 0.82% in the healthy lifestyle were diagnosed. Favorable lifestyle was associated with a lower risk of dementia despite an unfavorable genetic risk profile.

Favorable lifestyle habits in this study included: no smoking, limiting alcohol consumption to moderate levels, regular physical activity and maintaining a healthy diet. Regular physical activity was defined as per the American Heart Association (AHA) guidelines: 150 minutes of moderate or 75 minutes of vigorous activity per week (or an equivalent combination). This level of exercise, along with a healthy lifestyle, has also been associated with lowered risk of stroke and cardiovascular disease. Moderate alcohol consumption was defined according to the US dietary guidelines: 14g/day or less for women and 28g/day or less for men. Healthy diet was based on the dietary recommendations for maintaining optimal cardiometabolic health: this included regular consumption of at least 4 of the 7 food groups which constitute a healthy diet6.

This study provides evidence to support the benefits of a healthy lifestyle in reducing risk of dementia, even in individuals who may be at a higher genetic risk of developing dementia, including AD.  These results reinforce the American Heart Association’s healthy lifestyle recommendations for a healthy heart and healthy brain.

 

References:

  1. https://www.alz.org/alzheimers-dementia/what-is-dementia
  2. MangialascheF,KivipeltoM,SolomonA, Fratiglioni L. Dementia prevention: current epidemiological evidence and future perspective. Alzheimers Res Ther. 2012;4(1)
  3. http://investors.biogen.com/news-releases/news-release-details/biogen-and-eisai-discontinue-phase-3-engage-and-emerge-trials
  4. https://www.novartis.com/stories/discovery/stopping-alzheimers-disease-it-starts
  5. Ilianna Lourida, PhD1,2; Eilis Hannon, PhD1; Thomas J. Littlejohns, PhD3; et al. Association of Lifestyle and Genetic Risk With Incidence of Dementia. JAMA. Published online, July 13, 2019.
  6. Dietaryandpolicyprioritiesfor cardiovascular disease, diabetes, and obesity: a comprehensive review. Circulation. 2016;133(2): 187-225
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Follow Your Heart But Take Your Mind With You: Insights on Vascular Dementia

Reem Waziry, MD, MPH, PhD

Cardiovascular diseases such as diabetes and hypertension are established risk factors for mild cognitive impairment (MCI) and vascular dementia (VD). Vascular pathology occurs alongside neurodegenerative disease pathology, and both are associated with interactive effects on the clinical presentation of VD1. Several cardiovascular risk factors of VD could be modified during the preclinical course of the disease during midlife rather than later in life or closer to VD onset2,3.

In this year at ISC19, Angela L. Jefferson reported results supporting that age-related aortic stiffness contributes to transmission of damaging pulsatility and reduction in blood flow. This contributes to blood brain barrier compromise, resulting in reduced cerebral perfusion and subsequent tissue damage4. Brain MRI results suggest that vascular dysregulation may drive neurodegeneration over time, possibly due to neurofibrillary tangle formation or synaptic degradation4.

Looking from another angle, Lawrence J. Fine presented on the interplay between CVD and VD in epidemiological studies. According to data from the American Heart Association, loss of a perfect cardiovascular health during midlife is concurrently associated with steep increase in risk of MCI and vascular dementia. A recent report from the Women Health Initiative Memory Study (WHIMS) assessed MCI and Parkinson’s disease (PD) in women with myocardial infarction (MI). The data suggests modest absolute numbers, but higher rates of MCI and Parkinson’s disease (PD) cases in women with myocardial infarction (MI) (adjusted HR for PD or MCI was 2.23, 95% CI 1.51 to 3.30)5.

Investigators of the SprintMind trial examined the effect of one or more intensive high blood pressure treatment than is currently recommended. SprintMind was a randomized controlled trial that compared intensive treatment (goal SBP < 120 mm hg) to standard treatment (goal SBP < 140 mm Hg). Patients with major CVD as strokes, diabetes and congestive heart failure were excluded. The results suggest that intensive blood pressure control causes no harm on cognition with actual reduction in MCI risk compared to standard treatment6.

Overall, these observations add novel insights on the association between CVD and VD. More data is needed to assess the extent to which CVD contributes to the occurrence of MCI and dementia in more diverse populations and over longer follow-up periods.

 

REFERENCES

  1. Yaffe, Kristine. “Prevention of cognitive impairment with intensive systolic blood pressure control.” Jama (2019).
  2. Gottesman, Rebecca F., et al. “Associations between midlife vascular risk factors and 25-year incident dementia in the Atherosclerosis Risk in Communities (ARIC) cohort.” Jama neurology 74.10 (2017): 1246-1254.
  3. Gottesman, Rebecca F., et al. “Association between midlife vascular risk factors and estimated brain amyloid deposition.” Jama 317.14 (2017): 1443-1450.
  4. Jefferson, Angela L., et al. “Higher Aortic Stiffness Is Related to Lower Cerebral Blood Flow and Preserved Cerebrovascular Reactivity in Older Adults.” Circulation 138.18 (2018): 1951-1962.
  5. Haring, Bernhard, et al. “Cardiovascular Disease and Cognitive Decline in Postmenopausal Women: Results from the Women’s Health Initiative Memory Study.” Journal of the American Heart Association 2.6 (2013): e000369.
  6. Williamson, Jeff D. “A randomized trial of intensive versus standard systolic blood pressure control and the risk of mild cognitive impairment and dementia: results from SPRINT MIND.” Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association 14.7 (2018): P1665-P1666.