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Methods We conducted a bidirectional two-sample mendelian randomization study to see the correlation between three WM phenotypes —white matter hyperintensities, fractional anisotropy, and mean diffusivity — among three WM phenotypes — with AD using summary results from genome-wide association studies —with AD using summary results from genome-wide association studies. Results Over all MR techniques, there was no conclusive evidence linking WM MRI markers on AD. We found ample evidence of causal connections of AD on the risk of WMH. The causal effect of AD on WMH and MD disappeared when we discarded the single nucleotide polymorphisms near the APOE regions, indicating that AD's ability to raise the risk of white matter damage could be mitigated by APOE to some extent. However, our study showed that the underlying mechanisms relating AD and white matter lesions could be correlated to SNPs in APOE regions.
Source link: https://doi.org/10.1007/s40120-022-00353-9
Applying bioinformatics methods to study the differentially co-expressed genes helps us achieve our goals to discover new therapeutic targets. We first used gene expression omnibus databases to determine differentially expressed genes in this research. The enrichment of pivotal genes, such as gene ontology and pathway signaling, continued to evolve. In addition, the related protein–protein interaction network was also developed. A series of 712, 630, 487, and 997 genes were differentially identified in T2DM with microvascular disease and AD, with microvascular dysfunction and AD at incipient, moderate, and severe, respectively. AD and T2DM are closely related to microvascular disorders, according to a bioinformatics review, immune-related biological functions and pathways closely associate AD and T2DM. Further investigation into the regulatory factors that surround CACNA2D3, NUMB, and IER3 in the neuroendocrine field may lead to a promising direction for determining future comorbidity strategies.
Source link: https://doi.org/10.1007/s10528-021-10154-8
Alzheimer's disease is the most common cause of dementia among elderly adults. 7-Methoxytacrine is one of the approved drugs for the treatment of this disease. The drug amount in nanocapsules has been estimated at 65%. The average particle size of the 7-MEOTA@PCL nanocapsules was 237 nm, with a polydispersity index of 0. 31 and negative surface charge. The controlled release of the 7-METOTA from the polycaprolactone nanocapsules was demonstrated by in vitro release experiments. The drug was distributed under Fick's law, according to the application of the Korsmeyer–Peppas model to the release kinetics results.
Source link: https://doi.org/10.1007/s10924-021-02349-2
Cognitive stimulation, cognitive enhancement, and cognitive rehabilitation are all examples of cognitive training, cognitive preparation, and cognitive rehabilitation. After short, medium, or long-term interventions and depression after short-term intervention, cognitive training may have shown significant improvements in global cognitive function. However, after intervention ended, the positive effects of the intervention on general cognitive function or depression didn't seem to persist. The absence of evidence-backed and consistent conclusions regarding cognitive stimulation and cognitive training, cognitive training for memory, or other non-cognitive outcomes are also lacking.
Source link: https://doi.org/10.1007/s11065-021-09486-4
Alzheimer's disease is the most common cause of dementia, and mild cognitive impairment is considered the transitional state to AD dementia and other forms of dementia, whose symptoms are accompanied by impaired eye movement. Both prosaccade and antisaccade paradigms distinguished patients with ADD and MCI from controls, but antisaccade techniques were more effective than prosaccade techniques in distinguishing patients from controls, according to the author, however, antisaccade paradigms were more efficient than prosaccade paradigms in distinguishing patients from controls. Patients with ADD had significantly longer latencies than those with MCI during prosaccade, and the pattern was similar in second, when patients with ADD had significantly longer latencies than those with MCI, and antisaccade in the gap condition as patients with ADD had significantly more errors than patients with MCI. Both patients had similar symptoms, and the degree of the gap effect varied among healthy controls and MCI and ADD subjects, but the latency stayed high in both patients.
Source link: https://doi.org/10.1007/s11065-021-09495-3
Alzheimer's disease is the most common cause of cognitive impairment and dementia in older people around the world. We conducted a comprehensive targeted review of AD in North America, Europe, and Asia to gain a deeper grasp of the recent literature on AD, as well as those of mild cognitive impairment due to AD. Although patient- and proxy-rated QoL are highly correlated in patients with early AD dementia, proxy-rated QoL decreases more strongly as severity rises. The adherence of self-reported QoL in patients with more advanced AD dementia may be due to a lack of knowledge or to adaptation to circumstances. MCI is associated with a higher cost burden than people with normal cognition, and MCI patients with MCI have higher QoL.
Source link: https://doi.org/10.1007/s40120-022-00335-x
Methods BAN2401-201 trial results and published literature used to determine the long-term clinical outcomes of lecanemab for patients with early AD [i. e. , mild cognitive impairment due to AD and mild AD dementia] in patients with early AD [i. e. , mild cognitive impairment as a result of AD and mild AD dementia] on the basis of BAN2401-G000-201 trial findings and published literature. Results Lecanemab treatment was shown to reduce the rate of disease progression, resulting in an extended MCI course due to AD and mild AD dementia, as well as shorter durations of moderate and severe AD dementia. Patients in the lecanemab + SoC group were older for mild, moderate, and severe AD dementia in the Lecanemab + SoC group longer than for patients in the SoC group by 2. 51, 3. 13, and 2. 34 years, respectively. Conclusions Lecanemab's research shows the promise of lecanemab for patients with early AD, as well as how it can reduce disease progression and reduce the lifetime risk of institutionalized care.
Source link: https://doi.org/10.1007/s40120-022-00350-y
Mild cognitive impairment due to AD can lead to AD dementia; AD dementia etiology among patients with MCI can range from 40% to 75%, depending on the populations studied and whether the MCI diagnosis was made clinically or in combination with biomarkers. AD dementia risk increases with transition from normal cognition with no amyloid-beta accumulation to early neurodegeneration and then to MCI. The lifetime risk of AD dementia among women and 36 percent among men is expected to be 41. 9% among women and 33. 6% among males. Although preliminary results on transition from preclinical AD to MCI are scant, an review of change among the three preclinical National Institute on Aging and Alzheimer's Association stages indicates that NIA-AA stage 3 might be useful in conjunction with other treatment decision-making tools.
Source link: https://doi.org/10.1007/s40120-022-00338-8
Given the uncertain benefits and high cost of such treatments, commercial payers that eventually decide to pay aducanumab or other Alzheimer's disease treatments may require innovative payment methods to minimize their financial risk. These critical steps may help with the development of Alzheimer's disease in the long run, as well as providing a blueprint for more affordable novel therapies in other indications in the future.
Source link: https://doi.org/10.1007/s40273-022-01150-w
Alzheimer's disease is the most common cause of dementia and cognitive impairment, but there is currently no cure; however, there is currently no cure. A buildup of A, tau protein phosphorylation, oxidative stress, and AD inflammation is pathogenic, according to AD's AD. As the most effective therapeutic strategy for AD treatment, inhibiting A peptide aggregation has been suggested. SIRT1 transcriptional activation by Resveratrol-induced SIRT1 transcriptional stimulation is becoming more important in the development of novel therapeutic options for AD and other neurodegenerative disorders. We also discussed the therapeutic potential of resveratrol as an AD therapeutic agent that is safe against neurodegenerative disorders.
Source link: https://doi.org/10.1007/s12035-022-02859-7
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