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Relationship Between Depressive Disorders and Alzheimer’s Disease: A Longitudinal Study in Türkiye
Depressive disorders and Alzheimer’s disease are two of the most prevalent and disabling mentalhealth conditions worldwide, often co-occurring in older adults. This study aims to analyze theprevalence trends of depressive disorders and Alzheimer’s disease in Türkiye and globally from 1990to 2021, and to investigate the longitudinal relationship between these conditions within the Turkishpopulation. This study utilized Global Burden of Disease (GBD) 2021 data to assess annualprevalence and disability-adjusted life years (DALYs) for depressive disorders and Alzheimer’sdisease in Türkiye and worldwide from 1990 to 2021. Descriptive analyses were performed to identifytrends over time. To examine the long-term association between depression and Alzheimer’s diseasein Türkiye, Generalized Estimating Equations (GEE) were used, adjusting for age distribution tocontrol for confounding effects related to population aging. Global Alzheimer’s Prevalence in 2021was 720.49 per 100,000 (UI: 625.77–823.40), reflecting a 76% increase since 1990 (UI: 0.73–0.80).While, this situation in Türkiye was 823.35 (UI: 711.90–941.50), higher than the global rate. GlobalDALYs were 460.41 (UI: 218.43–974.14), showing an 81% increase (UI: 0.73–0.89). DALYs inTürkiye were 480.67 (UI: 235.18–1006.83), slightly above global levels, with a 96% increase (UI:0.72–1.19). Results of GEE indicated that, over time, higher levels or rates of depressive disorderswere associated with increased rates of Alzheimer’s disease in Türkiye. The global burden ofAlzheimer’s and depression is rising, with a slightly greater increase in Türkiye. This trend suggestsdepression may contribute to or signal early Alzheimer’s development. Policymakers should includedepression screening and treatment in dementia prevention programs. Addressing depression is notonly crucial for mental health but may also serve as a public health strategy to lessen Alzheimer’sdisease burden in Türkiye.</p
The therapeutic potential of Irisin in preventing fetal brain damage and cognitive deficits caused by maternal inflammation
In-vivo antioxidant and therapeutic effects of ellagic acid on ischemia-reperfusion injury in skeletal muscle
Aim: Skeletal muscle ischemia-reperfusion (IR) injury is a critical clinical issue characterized by oxidative stress, inflammation, and tissue damage, potentially leading to systemic organ dysfunction. Ellagic acid (EA), a naturally occurring polyphenolic compound, is widely recognized for its strong antioxidative, anti-inflammatory, and antiapoptotic effects demonstrated in various preclinical studies. This study sought to assess the therapeutic effects of EA in a rat model of lower extremity IR injury, focusing on histopathological and biochemical parameters. Material and Methods: 24 male Albino Wistar rats were randomly divided into four groups: Sham, EA, IR, and IR+EA. IR injury was induced by occluding the infrarenal abdominal aorta for 45 minutes, followed by 120 minutes of reperfusion. EA (40 mg/kg) was administered intraperitoneally prior to reperfusion. Left gastrocnemius muscle samples were collected for histopathological and biochemical analyses, including TOS, TAS, OSI, levels and PON-1 enzyme activity. Results: The IR group showed marked muscle injury, with a significantly higher total injury score (10.00±0.63) compared to the Sham (2.00±0.58) and EA groups (2.00±0.52) (p<0.001, both). The IR-EA group demonstrated notable improvement, with a reduced total injury score (6.17±0.54), which was also significantly lower than the IR group (p<0.001). Biochemically, TAS levels and PON-1 activity significantly decreased while TOS and OSI levels increased in the IR group compared to the sham and EA groups. In addition, EA treatment significantly increased TAS levels and PON-1 activity while reducing TOS and OSI levels in the IR-EA group compared to the IR group (p=0.039, p=0.045, p=0.045, p=0.007, respectively). Conclusion: EA effectively mitigated skeletal muscle damage induced by IR injury through its antioxidative, anti-inflammatory, and antiapoptotic mechanisms. The results suggest that EA exhibits potential effects as a therapeutic agent in managing IR-related injuries
Güncel Endodonti Çalışmaları 7
ENDODONTİK TEDAVİLERDE AĞRININ MEKANİZMASI VE ANALJEZİKLERİN ROLÜAğrı, Uluslararası Ağrı Araştırmaları Birliği (IASP) tarafından, “gerçek veya potansiyel doku hasarıyla ilişkili hoş olmayan duyusal ve duygusal bir deneyim” olarak tanımlanmaktadır. Diş hekimine başvuruların en yaygın nedenlerinden biri ağrıdır. Diş hekimi öncelikli olarak ağrıya neden olan patolojinin teşhisi yapılmalı, ardından uygun tedavi uygulanmalı ve ilaç kullanımı gerekli durumlarla sınırlandırılmalıdır. Diş ve çevre dokularla ilişkili ağrılar genellikle inflamasyon kaynaklıdır ve enfeksiyon, travma ya da cerrahi girişimler sonrası gelişebilir. Endodontik ağrı yönetimi, etkili bir endodontik tedavi ile uygun analjezik kullanımının kombinasyonunu içerir. Bu amaçla non-narkotik analjezikler (parasetamol, NSAİİ) ve narkotik analjezikler (opioidler) kullanılmaktadır. NSAİİ’ler, COX-1 ve COX-2 enzimlerini inhibe ederek prostaglandin sentezini azaltır ve inflamasyona bağlı ağrıyı etkili bir şekilde kontrol altına alır. İbuprofen, flurbiprofen, deksketoprofen, naproksen sodyum, etodolak ve diklofenak bu gruptadır ve en sık tercih edilen ilaçlardan biri ibuprofendir. Parasetamol ise güçlü analjezik ve antipiretik özelliklere sahip olup antiinflamatuar etkisi sınırlıdır. Opioidler, güçlü analjezik özellikleri nedeniyle bazı diş hekimliği uygulamalarında kullanılmakla birlikte, bağımlılık riski nedeniyle dikkatli reçetelendirilmelidir. Diş hekimliğinde ağrı yönetimi, farmakolojik ve klinik yaklaşımların birlikte uygulanmasını gerektirir.Anahtar Kelimeler: Ağrı Mekanizmaları, Ağrı Yönetimi, Analjezikler, Endodontik Ağrı, İnflamasyon, Non-steroid Antiinflamatuar İlaçlar, ParasetamolTHE MECHANISM OF PAIN AND THE ROLE OF ANALGESICS IN ENDODONTIC TREATMENTSPain is defined by the International Association for the Study of Pain (IASP) as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage”. One of the most common reasons for visiting the dentist is pain. The dentist should first diagnose the pathology causing the pain, then apply the appropriate treatment, and limit medication use to necessary cases.Pain related to the teeth and surrounding tissues is usually caused by inflammation and may develop due to infection, trauma, or surgical procedures. Endodontic pain management involves a combination of effective endodontic treatment and appropriate use of analgesics. For this purpose, non-narcotic analgesics (paracetamol, NSAIDs) and narcotic analgesics (opioids) are used. NSAIDs inhibit COX-1 and COX-2 enzymes, reducing prostaglandin synthesis and effectively controlling inflammation-related pain. Ibuprofen, flurbiprofen, dexketoprofen, naproxen sodium, etodolac, and diclofenac belong to this group, with ibuprofen being one of the most commonly preferred drugs.Paracetamol has strong analgesic and antipyretic properties, but its anti-inflammatory effect is limited.Opioids are used in some dental procedures due to their strong analgesic properties; however, they should be prescribed with caution due to the risk of addiction. Pain management in dentistry requires the combined application of pharmacological and clinical approaches.Keywords: Pain Mechanisms, Pain Management, Analgesics, Endodontic Pain, Inflammation, Non-steroidal Anti-inflammatory Drugs, Paracetamol</p
Prognostic markers in pheochromocytomas/paragangliomas: the role of histopathology, SDHB, MAML3 and MCM6 expression
Objective: There are currently no definitive prognostic markers that accurately predict malignant behavior in pheochromocytoma/paraganglioma (PCC/PGL). While metastasis develops in only 10–15% of adrenal-origin, this rate can rise up to 50% in those with extra-adrenal localization. This study aims to investigate the potential predictive effect of known histopathological features in PCC/PGL, alongside SDHB, S100, Ki-67 proliferation index, and the expression of MAML3 and MCM6 in predicting metastatic disease. Methods: The specimens of 71 patients who were diagnosed with PCC/PGL and underwent total excision between 2010 and 2021 were re-examined. Demographic, clinical, and histopathological data, as well as immunohistochemical results for Ki-67, S100, SDHB, MCM6, and MAML3, were recorded. Results: While distant organ metastasis was observed in 3.4% (n = 1/29) of PCC and 21.2% (n = 7/33) of head and neck PGL, this rate was found to be significantly higher at 66.7% (n = 6/9) in abdominal PGL (p 5.1 cm), the presence of > 3/10 HPF mitosis, and SDHB loss were associated with lower metastasis-free survival. While no conclusions could be drawn regarding MAML3, the prognostic value of MCM6 appears promising
Hydrogen Sulfide Alleviates Demyelination, Behavioral and Motor Impairments in a Cuprizone-Induced Rat Model of Multiple Sclerosis
Objectives: This study investigated the effects of the H2S donor sodium hydrosulfide (NaHS) on demyelination and behavioral deficits in a cuprizone (CPZ)-induced experimental rat model of MS. Methods: The rats were fed chow pellets supplemented with 1% CPZ for 5 weeks, and NaHS (50 and 100 μmol/kg) was administered during the last 2 weeks. For behavioral assessment, grip strength, passive avoidance, rota rod and elevated plus maze tests were performed. Nuclear factor kappa-B (NF-κB) and interleukin-1 beta (IL-1β) were measured to assess inflammation in brain tissue. Demyelination in the corpus callosum (CC) was assessed by immunohistochemistry for myelin basic protein (MBP), platelet-derived growth factor receptor α (PDGFRα) and Glial fibrillary acidic protein (GFAP). The TUNEL method was used to assess apoptosis. Results: Demyelination in the CC was reduced in the NaHS-treated groups. NaHS increased the amount of MBP and decreased the amount of PDGFRα and GFAP immunoreactive cells. NaHS reduced NF-κB, IL-1β levels, and the number of apoptotic cells in the brain tissue. In addition, NaHS improved muscle strength, motor coordination, learning and memory, and showed a significant anxiolytic effect. However, it was found that the beneficial effects of NaHS decreased at a high dose of 100 μmol/kg. Conclusion: H2S showed neuroprotective effects by reducing demyelination, inflammation and apoptosis in the CPZ-induced MS model. H2S also improved muscle strength, motor coordination, learning and memory and showed anxiolytic activity. Anti-inflammatory, anti-apoptotic and antioxidant effects may play a role in the neuroprotective effects of H2S