Strategic Cognitive Sequencing: A Computational Cognitive ...
Cognitive Decline, Dementia, Alzheimer's...
Transcript of Cognitive Decline, Dementia, Alzheimer's...
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Cognitive Decline, Dementia, Alzheimer's and….hope?Robert Adams D.O. AOBFP, IFMCP
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Declaration of Conflict of InterestsNone
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Objectives
1. Define cognitive impairment vs dementia vs Alzheimer's type dementia
2. Tools for assessing and defining cognitive decline and dementia
3. Social, economic burden of Alzheimer’s 4. Pathophysiology of Alzheimer's Dementia5. Discuss novel, intensive protocol demonstrating measures
of improvement.
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Cognitive Impairment
1. Change from baseline noticed by patient + knowledgeable informant + Clinical Cognitive Assessment Tool
2. Notice deficit in 1 of 5 settings a. Acquire & remember new informationb. Visual Spatialc. Reasoning/Judgment complex tasksd. Languagee. Personality behavior
3. Maintains independence in social and occupational functioning
4. Not due to other medical or psychological condition
Dementia1) Patient + knowledgeable informant + Clinical
Cognitive Assessment Tool2) Deficit in at least 2 of 5 settings
a) Acquire & remember new informationb) Visual Spatialc) Reasoning/Judgment complex tasksd) Languagee) Personality behavior
3) Interference with the ability to function at work or at usual activities
4) Not due to other medical or psychological condition
1. Albert MS, DeKosky ST, Dickson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011;7(3):270-9.2. McKhann GM, Knopman DS, Chertkow H, et al. The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011;7(3):263-9.3. Sperling, Reisa A. et al., Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimer's & Dementia: The Journal of the Alzheimer's Association , Volume 7 , Issue 3 , 280 - 292
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Cognitive Impairment
1. Change from baseline noticed by patient + knowledgeable informant + Clinical Cognitive Assessment Tool
2. Notice deficit in 1 of 5 settings a. Acquire & remember new informationb. Visual Spatialc. Reasoning/Judgment complex tasksd. Languagee. Personality behavior
3. Maintains independence in social and occupational functioning
4. Not due to other medical or psychological condition
SCI = Subjective Cognitive Impairment(Patient notices change)
MCI = Mild Cognitive Impairment(Patient and close associate notice change)
1. Albert MS, DeKosky ST, Dickson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011;7(3):270-9.2. McKhann GM, Knopman DS, Chertkow H, et al. The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011;7(3):263-9.3. Sperling, Reisa A. et al., Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimer's & Dementia: The Journal of the Alzheimer's Association , Volume 7 , Issue 3 , 280 - 292
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Clinical Cognitive Assessment tools per AOA online training-“On the Front lines with Alzheimer's Dementia: Diagnosis and Management”
Mini CogMontreal Cognitive Assessment (MoCA)St. Louis University Mental Status (SLUMS)
https://aoaonlinelearning.osteopathic.org/mod/page/view.php?id=674
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Mini cog! Clock drawing and 3 word
recall! Quick (2-3) min! Visuospatial, Word recall,
executive function! 0-2 high likelihood of dementia,
3-5 low likelihood of dementia
Simons, B. et al. Evaluation of suspected Dementia. Am Fam Physician. 2011 Oct 15;84(8):895-902.
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St Louis University Mental Status (SLUMS)
Approximately 10 min to administer
Orientation, short term memory, naming objects, calculations, clock drawing, geometric shape recognition
Scoring: See scaleEducation impacts scoring
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Montreal Cognitive Assessment (MOCA)10-15 min to administerTests visuospatial/executive, naming,
memory, attention, language, abstraction, delayed recall and orientation
26-30 is normal, 18-26 mild cognitive impairment, 11-17 mild dementia, 6-10 moderate dementia, <6 severe dementia
Sensitive for dementiaTechnical to administerEducational adjustment (+1 for high
school education or less)
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https://kateswaffer.com/2016/09/22/what-is-dementia-part-3/
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https://www.alzwisc.org/Types%20of%20dementia.htm https://gdblogs.shu.ac.uk/b2027135/2013/11/13/different-types-of-dementia/
https://qbi.uq.edu.au/brain/dementia/types-dementia
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Criteria for Alzheimer's: NIA-AADementia diagnosis with Insidious onset + Gradual worsening and:
Amnestic onset! Acquire and remember new information,
Personality, Behavior, Comportment
Evidence of CVD/stroke
Medical or neurologic Diagnosis affecting cognition
Medication affecting cognition
Features of non Alzheimer's Dementia
Non-Amnestic! Visiospatial, Language,
Reasoning, Judgement, Complex tasks
OR
Not in the setting of:
1.Albert MS, DeKosky ST, Dickson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011;7(3):270-9.2. McKhann GM, Knopman DS, Chertkow H, et al. The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011;7(3):263-9.3. Sperling, Reisa A. et al., Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimer's & Dementia: The Journal of the Alzheimer's Association , Volume 7 , Issue 3 , 280 - 292
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Dementia Diagnosis: NIA-AA
Alzheimer's & Dementia: The Journal of the Alzheimer's Association 2018 14, 535-562DOI: (10.1016/j.jalz.2018.02.018) Copyright © 2018 The Authors Terms and Conditions
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Alzheimer's & Dementia: The Journal of the Alzheimer's Association 2018 14, 535-562DOI: (10.1016/j.jalz.2018.02.018)
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This staging scheme reflects the sequential evolution of AD from an initial stage characterized by the appearance of abnormal AD biomarkers in asymptomatic individuals. As biomarker abnormalities progress, the earliest subtle symptoms become detectable. Further progression of biomarker abnormalities is accompanied by progressive worsening of cognitive symptoms, culminating in dementia
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6 Stages of Alzheimer's
Stage 1:! Cognitive tests normal! Patient-no decline in cognition/neurobehavior sx! Observer-no decline in cognition/neurobehavioral sx
Stage 2! Cognitive tests normal! Decline in previous level of cognition noted by patient or
observer! May have neurobehavioral symptoms! No functional impact on daily life Alzheimer's & Dementia: The Journal of
the Alzheimer's Association 2018 14, 535-562DOI: (10.1016/j.jalz.2018.02.018)
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6 stages of Alzheimer's (cont)Stage 3! Cognitive tests show impairment! Decline in previous level of cognition noted by patient or
observer! Cognitive presentation may not be primarily amnestic! Performs daily activities independentlyStage 4! Mild dementia! Substantial progressive cognitive impairment noted by
observer and/or patient! Clearly evident functional impact on daily life
Alzheimer's & Dementia: The Journal of the Alzheimer's Association 2018 14, 535-562DOI: (10.1016/j.jalz.2018.02.018)
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6 stages of Alzheimer's (cont)
Stage 5! Moderate dementia! Progressive cognitive/neurobehavioral impairment ○ Extensive impact on daily life○ Requires frequent assistance
Stage 6! Severe dementia! Progressive cognitive/neurobehavioral impairment○ Interview may not be possible○ Complete dependence in basic activities
Alzheimer's & Dementia: The Journal of the Alzheimer's Association 2018 14, 535-562DOI: (10.1016/j.jalz.2018.02.018)
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MRI - Magnetic resonance imaging
https://www.progressnp.com/article/neuroimaging-dementia-update-general-clinician/
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FDG-PET Scan(Fluorodeoxyglucose Positron Emission Tomography Scan)
PET scans can detect the decline in glucose metabolism associated with decreased cognitive function, particularly in the temporal and parietal lobes located on the sides and the back of the brain, the regions associated with memory formation and language. UCBerkeley researchers are finding that brain imaging shows promise as a method of detecting early signs of Alzheimer's disease. On the left is a PET scan showing normal levels of glucose metabolism, indicated in yellow and red. The levels of glucose metabolism in the brain are decreased in patients with mild cognitive impairment (middle) and with Alzheimer's disease (right).Credit: Cindee Madison and Susan Landau, UC Berkeley
https://www.sciencedaily.com/releases/2009/07/090714085812.htm
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Am-PET Scan(Amyloid Positron Emission Tomography Scan)
Amyloid PET scanning makes amyloid plaques "light up" on a brain PET scan, enabling, for the first time, accurate detection of plaques in living people.
https://radiology.ucsf.edu/patient-care/services/specialty-imaging/alzheimer
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https://www.youtube.com/watch?time_continue=43&v=NjgBnx1jVIUBredesen DE (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707-717
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Quick facts(Patient statistics)
https://alz.org/alzheimers-dementia/facts-figures
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Caregivers
https://alz.org/alzheimers-dementia/facts-figures
Eighty-three percent of the help provided to older adults in the United States comes from family members, friends or other unpaid caregivers. Nearly half of all caregivers who provide help to older adults do so for someone with Alzheimer's or another dementia.
Who are the caregivers?
● About one in three caregivers (34 percent) is age 65 or older.● Approximately two-thirds of caregivers are women; more
specifically, over one-third of dementia caregivers are daughters.
● Approximately one-quarter of dementia caregivers are "sandwich generation" caregivers — meaning that they care not only for an aging parent, but also for children under age 18.
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While there is no cure for Alzheimer’s disease or a way to stop or slow its progression, there are drug and non-drug options that may help treat
symptoms. Understanding available options can help individuals living with the disease and their caregivers to cope with symptoms and improve
quality of life.
https://www.alz.org/alzheimers-dementia/treatments
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Extensive preclinical studies from numerous laboratories have identified multiple pathogenetic targets for potential intervention. These include, in addition to amyloid-β (Aβ) oligomers and tau, inflammatory mediators, apolipoproteins and lipid metabolism factors, hormonal mediators, trophic factors and their receptors, calcium regulatory pathways, axoplasmic transport machinery, neurotransmitters and their receptors, prion protein, and a host of other potential targets. However, one of the drawbacks of these preclinical studies is that many have implicated single pathways, and shown large effects of targeting one pathway, whereas in human studies, such approaches have not been borne out.
Bredesen DE (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707-717.
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There are several possible inferences from such discrepant results:
! first, it is possible that it will be necessary to target multiple pathways simultaneously in order to effect an improvement in symptoms and pathophysiology.
! Second, it is possible that targeting a single pathway will be sufficient, but that earlier intervention will be required.
! Third, it is possible that all of these seemingly disparate pathways will converge on a single critical pathway, so that either a single targeted therapy or a multi-component, multi-targeted approach may be effective.
! And fourth, of course it is possible that neither of these two types of approaches will be sufficient.
Bredesen DE (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707-717.
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While there is no cure for Alzheimer’s disease or a way to stop or slow its progression, there are drug and non-drug options that may help treat
symptoms. Understanding available options can help individuals living with the disease and their caregivers to cope with symptoms and improve
quality of life.
https://www.alz.org/alzheimers-dementia/treatments
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The Tenets of Osteopathic Medicine express the underlying philosophy of osteopathic medicine and were approved by the AOA House of Delegates as policy.
1. The body is a unit; the person is a unit of body, mind, and spirit.
2. The body is capable of self-regulation, self-healing, and health maintenance.
3. Structure and function are reciprocally interrelated.
4. Rational treatment is based upon an understanding of the basic principles of body unity, self-regulation, and the interrelationship of structure and function.
https://osteopathic.org/about/leadership/aoa-governance-documents/tenets-of-osteopathic-medicine/
Tenets of Osteopathic
Medicine
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The Tenets of Osteopathic Medicine express the underlying philosophy of osteopathic medicine and were approved by the AOA House of Delegates as policy.
1. The body is a unit; the person is a unit of body, mind, and spirit.
2. The body is capable of self-regulation, self-healing, and health maintenance.
3. Structure and function are reciprocally interrelated.
4. Rational treatment is based upon an understanding of the basic principles of body unity, self-regulation, and the interrelationship of structure and function.
https://osteopathic.org/about/leadership/aoa-governance-documents/tenets-of-osteopathic-medicine/
Tenets of Osteopathic
Medicine
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Based on a combination of in vitro and in vivo studies, we have advanced a model in which AD results from an imbalance in endogenous plasticity signaling (Fig. 1), [5-9], and in which the β-amyloid precursor protein (APP) is a mediator of such plasticity-related signaling.
Bredesen DE (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707-717.
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Bredesen DE (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707-717.
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Bredesen DE (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707-717.
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The patient began on the following parts of the overall therapeutic system: (1) he fasted for a minimum of 3 hours a between dinner and bedtime, and fo a minimum of 12 hours between dinner and breakfast: (2) he eliminated simple carbohydrates and processed foods from his diet; (3) he increased consumption of vegetables and fruits, and limited consumption of fish to non-farmed, and meat to occasional grass-fed beef or organic chicken; (4) he took probiotics; (5) he took coconut oil i tsp bid; (6) he exercised strenuously, swimming 3-4 times a week; (7) he took melatonin 0.5 mg po qhs, and tried to sleep as close to 8 hours per night as his schedule would allow; (8) he took herbs Bacopa monniera 250 mg, Ashwaganda 500mg, and tumeric 400 mg each day; (9) he took Methylcobalamin 1 mg, methyltetrahydrofolate 0.8mg, and pyridoxine-5-phosphate 50 mg po bid; (11) he took vitamin C 1 g per day, Vitamin D3 5000IU per day, vitamin E 400Iu per day, CoQ10 200 mg per day, Zn picolinate 50 per day, and alpha-lipoic acid 100 mg per day; (12) he took DHA 320mg and EPA 180 mg per day.
Bredesen DE (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707-717.
A day in the life with the protocol
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Obstacles to treatment
Bredesen DE (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707-717.
https://www.pinterest.com/pin/412994228306464692/?lp=true
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Bredesen DE (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707-717.
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1. Cognitive Traininga. Interventions aimed at enhancing
reasoning, memory, and speed of processing, to delay or slow age-related cognitive decline were found promising
2. Blood Pressurea. particularly in midlife, might prevent,
delay or slow clinical Alzheimer’s-type dementia
3. Physical Activitya. Citing the many known health
benefits of physical activity, the committee pointed to growing evidence that among these is the possible reduced risk of age-related cognitive decline
https://www.nih.gov/news-events/news-releases/national-academies-committee-sees-promising-inconclusive-evidence-interventions-prevent-cognitive-decline-dementia
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Bredesen et al. (2018) Reversal of Cognitive Decline:100. J Alzheimers Dis Parkinsonism 2018, 8:5
Bredesen DE (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707-717.
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Bredesen et al. (2018) Reversal of Cognitive Decline:100. J Alzheimers Dis Parkinsonism 2018, 8:5
This model suggests that the probability of developing Alzheimer’s disease is proportional to the ratio of synaptoclastic signaling to synaptoblastic signaling.
Some examples include: 1. Identifying and treating pathogens such as Borrelia, Babesia,
or Herpes family viruses:2. Identifying gastrointestinal hyperpermeability, repairing the
gut, a enhancing the microbiome;3. Identifying insulin resistance and protein glycation, and
returning insulin sensitivity and reduced protein glycation;4. Identify and correct suboptimal nutrient, hormone, or trophic
support (including vascular support);5. Identifying toxins (metallotoxins and other inorganics,
organic toxins, or biotoxins), reducing toxic exposure and detoxifying.
Since each patient has a different combination of the many potential contributors to cognitive decline, the approach to treatment is targeted and personalized.
Bredesen DE (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707-717.
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Outcomes
Bredesen et al. (2018) Reversal of Cognitive Decline:100. J Alzheimers Dis Parkinsonism 2018, 8:5
KeyAm-PET = Amyloid Positron Emission Tomography Scan
CNS-VS = CNS Vital Signs;
CVLT: California Verbal Learning Test
FDG-PET = Fluorodeoxyglucose Positron Emission Tomography Scan
HC = Hippocampus
MCI = Mild Cognitive Impairment
MMSE = Mini-Mental Status Exam
MoCA = Montreal Cognitive Assessment
NP = Neuropsychiatric testing
Age/Gender APOE status Symptom Diagnosis Imaging Cognitive measurement Outcome
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MRI - Magnetic resonance imaging
https://www.progressnp.com/article/neuroimaging-dementia-update-general-clinician/
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Quantitative analysis of brain structure volumes
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Discussion
Bredesen et al. (2018) Reversal of Cognitive Decline:100. J Alzheimers Dis Parkinsonism 2018, 8:5
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Discussion
Bredesen et al. (2018) Reversal of Cognitive Decline:100. J Alzheimers Dis Parkinsonism 2018, 8:5
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Discussion
Bredesen et al. (2018) Reversal of Cognitive Decline:100. J Alzheimers Dis Parkinsonism 2018, 8:5
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Controversie
Hellmuth J, Rabinovici GD, Miller BL. The Rise of Pseudomedicine for Dementia and Brain Health. JAMA.2019;321(6):543–544. doi:10.1001/jama.2018.21560
-https://jamanetwork.com/journals/jama/article-abstract/2723294
Recently, detailed protocols to reverse cognitive changes have been promoted, but these protocols merely repackage known dementia interventions (eg, cognitive training, exercise, a heart healthy diet) and add supplements and other lifestyle changes. Such protocols are promoted by medical professionals with legitimate credentials, offer a unique holistic and personal approach and are said to be based on rigorous data published in reputable journals. However, when examining the primary data, the troubling and familiar patterns of testimony and cargo cult science emerge. The primary scientific articles superficially appear valid, yet lack essential features, such as sufficient participation characterization, uniform interventions, or treatment randomization with control or placebo groups, and may fail to include sufficient study limitations. Some of these poor-quality studies may be published in predatory open access journals.”
“A similarly concerning category of pseudomedicine involves interventions promoted licensed medical professionals that target unsubstantiated etiologies of neurodegenerative disease (eg, metal toxicity; mold exposure’ infectious causes, such as Lyme disease).”
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Controversie - moreThe possibility that Alzheimer’s disease (AD) has a microbial etiology has been proposed by several researchers. Here, we provide evidence that tissue from the central nervous system (CNS) of AD patients contain fungal cells and hyphae….Different brain regions including external frontal cortex, cerebellar hemisphere, entorhinal cortex/hippocampus and choroid plexus contain fungal material, which is absent in brain tissue from control individuals. Analysis of brain sections from ten additional AD patients reveals that all are infected with fungi….Sequencing of fungal DNA extracted from frozen CNS samples identifies several fungal species. Collectively, our findings provide compelling evidence for the existence of fungal infection in the CNS from AD patients, but not in control individuals.
Pisa, D. et al. Different Brain Regions are Infected with Fungi in Alzheimer's Disease. Sci. Rep. 5, 15015; doi: 10.1038/srep15015 (2015).
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Conclusion1. Cognitive Decline is on a continuum with dementia and there are several
different diagnoses that lead to dementia. 2. Alzheimers dementia is the most common cause of dementia and leads to
general decline of cognition.3. The social impacts are significant and the economic burdens are expected to
increase.4. This has been an untreatable disease that has not responded to monotherapy
interventions5. Therapeutic intervention systems directed at decreasing insulting signals and
increasing the trophic signals for amyloid precursor protein (APP) have shown some favorable changes in symptoms with some patients having Alzheimer's dementia.
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ReferencesAlbert MS, DeKosky ST, Dickson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011;7(3):270-9.
McKhann GM, Knopman DS, Chertkow H, et al. The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. 2011;7(3):263-9.
Sperling, Reisa A. et al., Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimer's & Dementia: The Journal of the Alzheimer's Association , Volume 7 , Issue 3 , 280 - 292
https://aoaonlinelearning.osteopathic.org/mod/page/view.php?id=674
Simons, B. et al. Evaluation of suspected Dementia. Am Fam Physician. 2011 Oct 15;84(8):895-902.
https://www.alzwisc.org/Types%20of%20dementia.htm
https://gdblogs.shu.ac.uk/b2027135/2013/11/13/different-types-of-dementia/
https://qbi.uq.edu.au/brain/dementia/types-dementia
Bredesen DE (2014) Reversal of cognitive decline: A novel therapeutic program. Aging 6: 707-717
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Referenceshttps://www.youtube.com/watch?time_continue=43&v=NjgBnx1jVIU
https://alz.org/alzheimers-dementia/facts-figures
https://www.alz.org/alzheimers-dementia/treatmentshttps://osteopathic.org/about/leadership/aoa-governance-documents/tenets-of-osteopathic-medicine
https://www.nih.gov/news-events/news-releases/national-academies-committee-sees-promising-inconclusive-evidence-interventions-prevent-cognitive-decline-dementia
Bredesen et al. (2018) Reversal of Cognitive Decline:100. J Alzheimers Dis Parkinsonism 2018, 8:5
https://www.sciencedaily.com/releases/2009/07/090714085812.htm
https://radiology.ucsf.edu/patient-care/services/specialty-imaging/alzheimer
https://www.progressnp.com/article/neuroimaging-dementia-update-general-clinician/
https://kateswaffer.com/2016/09/22/what-is-dementia-part-3/
Pisa, D. et al. Different Brain Regions are Infected with Fungi in Alzheimer's Disease. Sci. Rep. 5, 15015; doi: 10.1038/srep15015 (2015).
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References
Alzheimer's & Dementia: The Journal of the Alzheimer's Association 2018 14, 535-562DOI: (10.1016/j.jalz.2018.02.018)
Hellmuth J, Rabinovici GD, Miller BL. The Rise of Pseudomedicine for Dementia and Brain Health. JAMA.2019;321(6):543–544. doi:10.1001/jama.2018.21560
-https://jamanetwork.com/journals/jama/article-abstract/2723294