How Is Alzheimers Disease Treated
Medical management can improve quality of life for individuals living with Alzheimers disease and for their caregivers. There is currently no known cure for Alzheimers disease. Treatment addresses several areas:
- Helping people maintain brain health.
- Managing behavioral symptoms.
- Slowing or delaying symptoms of the disease.
Crosstalk Of T2dm And A Pathology In Ad
One of the hallmarks of AD pathology is the formation of extracellular amyloid plaques composed of insoluble deposits of amyloid- protein aggregates. A is generated from the proteolytic cleavage of amyloid precursor protein by a sequence of enzymatic reactions from BACE-1, and -secretase complex . It is hypothesized that lower concentration of A remains in the soluble form and subject to clearance after degradation, while higher concentrations aggregate into insoluble plaques that are resistant to degradation . While there is no evidence that AD brains secrete more soluble A than normal brains, a recent body of evidence suggests that an increased accumulation of insoluble A plaques arise due to impaired clearance of A protein .
Pathology Studies: Islet Amyloid In Alzheimer Disease And Brain Amyloid In Type 2 Diabetes
Protocol 3: islet amyloid in Alzheimer disease.
Both the frequency and the extent of islet amyloid were higher in the Alzheimer disease group versus the non-Alzheimer disease group despite a trend toward a lower BMI in Alzheimer disease . As expected, the frequency and the extent of islet amyloid was greater in type 2 diabetes versus non-type 2 diabetes .
Inclusion of cases in this autopsy protocol was blinded with respect to the presence or absence of diabetes but with the requirement that FPG be documented. Subsequent analysis of the FPG concentrations revealed that the prevalence of type 2 diabetes in the Alzheimer disease group was 32% and in non-Alzheimer disease cases was 14% . The mean FPG in Alzheimer disease was not higher than in control subjects .
Protocol 4: brain amyloid in type 2 diabetes.
The density of diffuse or neuritic plaques or NFT was not different between patients with type 2 diabetes versus nondiabetic control subjects . As expected, the density of neuritic plaques, diffuse plaques, and NFT was greater in Alzheimer disease cases versus non-Alzheimer disease .
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What To Do If A Loved One Is Suspicious Of Having Dementia
- Discuss with loved one. Talk about seeing a medical provider about the observed changes soon. Talk about the issue of driving and always carrying an ID.
- Medical assessment. Be with a provider that you are comfortable with. Ask about the Medicare Annual Wellness exam.
- Family Meeting. Start planning, and gather documents like the Health Care Directive, Durable Power of Attorney for Health Care, Estate Plan.
Total Cost Of Health Care And Long
Table reports the average annual per-person payments for health care and long-term care services for Medicare beneficiaries age 65 and older with and without Alzheimer’s or other dementias. Total per-person health care and long-term care payments in 2019 from all sources for Medicare beneficiaries with Alzheimer’s or other dementias were over three times as great as payments for other Medicare beneficiaries in the same age group .,
|TOTAL* Payments from sources do not equal total payments exactly due to the effects of population weighting. Payments for all beneficiaries with Alzheimer’s or other dementias include payments for community-dwelling and facility-dwelling beneficiaries.||50,201||14,326|
- * Payments from sources do not equal total payments exactly due to the effects of population weighting. Payments for all beneficiaries with Alzheimer’s or other dementias include payments for community-dwelling and facility-dwelling beneficiaries.
- Created from unpublished data from the Medicare Current Beneficiary Survey for 2011.
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How Is Dementia Treated
Treatment of dementia depends on the underlying cause. Neurodegenerative dementias, like Alzheimers disease, have no cure, though there are medications that can help protect the brain or manage symptoms such as anxiety or behavior changes. Research to develop more treatment options is ongoing.
Leading a healthy lifestyle, including regular exercise, healthy eating, and maintaining social contacts, decreases chances of developing chronic diseases and may reduce number of people with dementia.
What You Can Do Now
While more research needs to be done to confirm the relationship between the two diseases we know that eating healthy can keep diabetes away, which may keep Alzheimers away. The study also showed that losing weight and exercising may keep the early stages of Alzheimers at bay.
The following lifestyle changes can keep you from developing type 2 diabetes:
- Eat healthy
- Regular exercise
- Quit smoking
Were you aware about the connection between Alzheimers and diabetes? Will you change your health for body and mind? Share your thoughts with us in the comments below.
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Trends In Dementia Caregiving
There is some indication that families are now better at managing the care they provide to relatives with dementia than in the past. From 1999 to 2015, dementia caregivers were significantly less likely to report physical difficulties and financial difficulties related to care provision. In addition, use of respite care by dementia caregivers increased substantially . However, as noted earlier, more work is needed to ensure that interventions for dementia caregivers are available and accessible to those who need them. A 2016 study of the Older Americans Act’s National Family Caregiver Support Program found that over half of Area Agencies on Aging did not offer evidence-based family caregiver interventions.
What Are The Most Common Types Of Dementia
- Alzheimers disease. This is the most common cause of dementia, accounting for 60 to 80 percent of cases. It is caused by specific changes in the brain. The trademark symptom is trouble remembering recent events, such as a conversation that occurred minutes or hours ago, while difficulty remembering more distant memories occurs later in the disease. Other concerns like difficulty with walking or talking or personality changes also come later. Family history is the most important risk factor. Having a first-degree relative with Alzheimers disease increases the risk of developing it by 10 to 30 percent.
- Vascular dementia. About 10 percent of dementia cases are linked to strokes or other issues with blood flow to the brain. Diabetes, high blood pressure and high cholesterol are also risk factors. Symptoms vary depending on the area and size of the brain impacted. The disease progresses in a step-wise fashion, meaning symptoms will suddenly get worse as the individual gets more strokes or mini-strokes.
- Lewy body dementia. In addition to more typical symptoms like memory loss, people with this form of dementia may have movement or balance problems like stiffness or trembling. Many people also experience changes in alertness including daytime sleepiness, confusion or staring spells. They may also have trouble sleeping at night or may experience visual hallucinations .
Confounding Of The Association
Cardiovascular risk factors such as smoking , hypertension , hyperlipidemia , and obesity have been associated with AD previously. Clustering of hyperglycemia, hypertension, hyperlipidemia, and obesity comprises the metabolic syndrome, a condition found in more than 20% of the American population . Because of the independent association of these risk factors with AD and their tendency to occur in clusters, studies that have not properly adjusted for these covariates are highly susceptible to confounding. Although most studies adjusted for age and sex, less than half adjusted for vascular risk factors . Interestingly, results from our subgroup analysis demonstrated that adjusting for cardiovascular risk factors increased the risk estimate. This suggests that T2DM is more likely to be involved in the pathogenesis of AD than associated through a spurious relationship.
New Insight Into The Alzheimers And Diabetes Connection
The link between Alzheimers and diabetes continues to grow stronger with a new paper by Professor Melissa Schilling, a strategy and innovation expert at the NYU Stern School of Business. The paper, recently published in The Journal of Alzheimers Disease, found that hyperinsulinemia, caused by early or undiagnosed diabetes, obesity or prediabetes is also found in nearly half of all people with Alzheimers. Schilling reviewed hundreds of published articles about the pathway between insulin and Alzheimers, leading her to a new understanding of the connections between the two disease. She said:
What Ive learned from my innovation research is that specialists can become trapped in the logic of their field, so new perspectives often come from outsiders. If we can raise awareness and get more people tested for hyperinsulinemia, especially those who have been diagnosed with or who are at risk for dementia, it could significantly lessen the incidence of Alzheimers disease and vascular dementia, as well as other diabetes-related health problems.
Her findings could have major implications for Alzheimers and diabetes detection, including,
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Impact Of Hyperglycemia On Other Posttranslational Modifications Of Tau
Acetylation is a post translational modification in which the acetyl group from acetyl CoA is reversibly transferred to lysine amino group in the tau protein. This process is modulated by acetyltransferases and deacetylases . Cohen et al. observed that tau acetylation at the key lysine residues at K/163/280/281/369 was crucial for tau-microtubule binding interactions and microtubule stabilization. Using cellular and transgenic mouse models as well as human brains from a wide spectrum of tauopathies this group has demonstrated that tau acetylation disrupts the tau-microtubule binding interactions and promotes pathological tau aggregation. This group further demonstrated that acetylated tau was associated with the formation of insoluble tau NFTs in tau transgenic mice and human tauopathies indicating acetylation as a pathogenic post-translational modification of tau .
Although it is still speculative, it has been hypothesized that abnormal glucose metabolism in the brain induced by T2DM may lead to decreased brain O-GlcNAc levels. This reflects a failure in the neuroprotective mechanism in the brain and triggers the cascade of tau pathology enabling disease progression.
Lowering The Risk Of Alzheimers Disease
These findings are exciting because they show more conclusively than ever before that there are things we can do, especially regarding cardiovascular disease risk factors, to reduce our risk of mild cognitive impairment and dementia. – Maria C. Carrillo, Ph.D., Sprint for Discovery: New Dementia and Cardiovascular Findings, Alzheimers Association Twitter:
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How Can Family Members Support Someone With Dementia
Communicate comfort verbally and physically to a person. The distraction of a large number or redirection of a child could also work. Your loved one might find that working for you and folding laundry helps her feel useful and useful by helping to keep her busy. This condition increases the tendency for people with dementia to refuse or become resistant to activities such as bathing and dressing.
Alarming Statistics On Anxiety Disorders
Anxiety is a common mental health issue for all developed countries around the world. As the workplace and schools put increasing amount of stress on both adults and children in the society, how detrimental is this growing anxiety issue to the mental and physical health of each individual, and how does it affect the society as a whole? Here are 50 alarming statistics on anxiety disorders that will make you rethink about your anxiety level and your mental wellness.
Inflammation And Ad Pathology
Recently preclinical, genetic, and bioinformatics studies have shown that the immune system activation accompanies AD pathology. The genome wide association studies between AD and rare mutations in the genes encoding triggering receptor expressed on myeloid cells 2 and myeloid cell surface antigen CD33 provide clear evidence that there is a strong linkage between alterations in the immune system and the progression of AD pathology .
A and Inflammation
Recently a huge repertoire of GWAS studies show that structural variants of genes encoding immune receptors TREM2, CD33, and CR1, all of which are expressed in the microglia confer higher risk of AD . However, the function of TREM2 deficiency in the progression of AD has been controversial. For instance, while TREM2 deficiency in APP/PS1 mice ameliorated hippocampal A accumulation the 5XFAD mice displayed an opposite result. In these mice the A pathology was found to develop slower than APP/PS1 mice and increased accumulation of hippocampal A was observed in the absence of TREM2 . Elevated levels of soluble TREM2 was detected in the CSF of early AD patients suggesting a change in microglial activation in response to neuronal death. Although the exact mechanism still remains to be deciphered, these findings show that impaired TREM2 function plays a vital role in A-mediated AD pathogenesis.
Tau and Inflammation
Post Traumatic Stress Disorder
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Risk Factors And Prevention
Although age is the strongest known risk factor for dementia, it is not an inevitable consequence of biological ageing. Further, dementia does not exclusively affect older people young onset dementia accounts for up to 9% of cases. Studies show that people can reduce their risk of cognitive decline and dementia by being physically active, not smoking, avoiding harmful use of alcohol, controlling their weight, eating a healthy diet, and maintaining healthy blood pressure, cholesterol and blood sugar levels. Additional risk factors include depression, social isolation, low educational attainment, cognitive inactivity and air pollution.
Inflammation And Blood Vessel Damage
With diabetes, you’re at greater risk for a heart attack or stroke. And high blood sugar levels can trigger inflammation. None of that is good for your blood vessels. Damaged vessels in your brain could lead to Alzheimer’s.
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The Correlation Between Alzheimers And Type 2 Diabetes
A new study done by researchers at Albany University in New York, shows that Alzheimers may be the late stages of type 2 diabetes.
People who have type 2 diabetes produce extra insulin. That insulin can get into the brain, disrupting brain chemistry and leading toxic proteins that poison brain cells to form. The protein that forms in both Alzheimers patients and people with type 2 diabetes is the same protein.
Researcher Edward McNay at Albany University, said:
People who develop diabetes have to realize this is about more than controlling their weight or diet. Its also the first step on the road to cognitive decline. At first they wont be able to keep up with their kids playing games, but in 30 years time they may not even recognize them.
Diagnosis Of Incident Dementia Alzheimers Disease And Vad
Further, the Alzheimers disease diagnoses were subdivided in two groups of Alzheimers disease cases with history of stroke , and Alzheimers disease cases in the absence of any current or past vascular diseases and diagnosed diabetes. Details of the reclassification procedure have been reported elsewhere .
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Impact Of Insulin Resistance On Tau Cleavage
In addition to hyperphosphorylation, another abnormal post-translational modification of tau is truncation. Tau is cleaved by a host of proteolytic enzymes including caspases, calpains, thrombins, and puromycin-sensitive amino peptidase. These truncated tau fragments lack both N terminal and C terminal fragments and form the core component of NFTs .
In AD brains, caspases are activated causing tau protein to be cleaved at several residues. The C-terminal cleavage of tau by caspase-3 gives rise to Asp421 residue that has a higher propensity of aggregation and is found to be associated with neurofibrillary pathology in AD brains. The presence of Asp421 truncated tau in the neurofibrillary aggregates observed in the neurons of double transgenic mice and in P301S mouse models of tauopathy indicates that the formation of Asp421 cleavage product is an important step toward formation and maturation of tau aggregates .