Exposure to repetitive head impacts (RHI) is associated with increased risk of a range of neurodegenerative diseases, including Alzheimer disease and amyotrophic lateral sclerosis. However, while the protein pathologies in the brains of individuals with the RHI-associated pathology of chronic traumatic encephalopathy (CTE) are well described, the spinal cord pathology in at-risk individuals remains poorly understood. To evaluate spinal cord pathologies associated with RHI exposure or CTE neuropathologic change (CTE-NC) in the brain. This case-control study of a retrospective autopsy series (June 2019 to August 2025) was performed among autopsied individuals who served as RHI-exposed cases or controls in a multicenter brain bank collaboration. Data analysis was performed from January 2024 to November 2025. RHI history and CTE-NC presence. Informant-reported clinical history as well as symptoms and immunohistochemistry for phosphorylated tau (p-tau), phosphorylated TAR DNA-binding protein 43 (p-TDP-43), α-synuclein, and amyloid-β (Aβ), as well as amyloid precursor protein and human leukocyte antigen DR. Of 70 autopsied individuals (62 male, 8 female; mean [SD] age, 64.40 [13.94] years), 20 showed CTE-NC in the brain. All cases with CTE-NC exhibited spinal cord p-tau deposits, especially in cases aged 65 years or older with prior RHI (n = 14), often showing extensive spinal tau pathology as both neuronal (all 14 cases) and astrocytic (12 of 14 cases [86%]) p-tau deposits. Spinal p-tau pathology was associated with microglial activation and motor symptoms. Notably, among the individuals with CTE-NC and prior RHI who were aged 65 years or older, additional spinal protein pathologies were present, comprising p-TDP-43 inclusions (9 of 14 cases [64%]), Aβ deposits (13 of 14 cases [93%]), and α-synuclein deposits (7 of 14 cases [50%]), with all 4 of these pathologies present in 4 individuals (29%). In total, across all 20 CTE-NC cases, p-TDP-43 inclusions were confined to the spinal cord in 5 of the 10 individuals with spinal p-TDP-43 pathology. In contrast, among 50 individuals without CTE-NC, typically sparse p-tau deposits were seen in only 27 (54%). Among the 23 confirmed cases with a history of RHI, 16 (70%) exhibited CTE-NC, while 7 (30%) did not. Spinal tau pathology was more severe in those with CTE-NC; however, astrocytic tau pathology was also present in the group without CTE-NC, unlike in controls without RHI or CTE. This case-control study provides autopsy evidence of a high prevalence of complex spinal pathology in individuals with CTE-NC, supporting the concept of trauma-related encephalomyelopathy. The frequent co-occurrence of p-TDP-43, Aβ, and α-synuclein pathologies in individuals aged 65 years or older with CTE-NC suggests that cumulative trauma might contribute to widespread misfolded protein aggregation.

Abstract Introduction: In 1957 spontaneous regression(SR) was established as most frequently in lymphomas, renal and melanoma and in 1968 used by MacFarlain Burnet, to suggest immune surveillance against cancer was a function of the immune system, and that the frequency was greater in earlier stages of cancer. In 1988 Renal cell cancer reported frequency was 6.6% in 73 cases. Despite SR reports increasing since the success of modern immunotherapeuty, a recent review found only 1 case of metastatic prostate cancer (PC) and there was no PC in a series of 58 cases of Radiation Abscopal response(RAR). Though fitting with PC’s reputation as a “cold” cancer, ie having a low response to modern immunotherapy (<5%), this abstract used alternative words in Urology literature to investigate further. Materials and Method: Three terms, evanescent, “vanished” and T0 were used in PUB med searches against second word Prostate.Active surveillance(AC) PC series with post entry biopsy data were also reviewed for incident of T0. Given the high incidence of obesity in series of PC, as additional evidence, we searched for GLP-1RA and PC. Results: The initial search revealed 16 cohorts of prostatectomy and found to have T0. The largest, Knipper, S. et al 2019, found 358/160,352(0.2%) were T0. Most had low volume disease but pT0 was identified in 13/358 (3.6%) with PSA ≥20 ng/ml, in 69 (19.3%) with biopsy GS ≥7 and in 78 (21.8%) with ≥cT2. In a subset, pT0 was identified in 34 (33.3%) patients with ≥2 positive biopsy cores. Eight series of AC with repeat biopsy revealed 952 T0/2862(33.3%), ranging from 41.45% in series with lowest relapse risk to 11.06% with highest relapse risk . Searching for association of GLP-1RA and Prostate cancer revealed a meta-analysis of 5 series of RR 0.72 (95% CI: 0.610 to 0.832). Conclusion: The Knipper et el series demonstrated SR in advanced Primary PC. The nem series in AS is the same as SR HPV positive pre-cancer of the Cervix and as reports of early Prostate cancer with HPV positive from Australia and Canada, investigation is need to see if T0 patients had HPV present. Autopsy series shows that earliest stages of PC precursors occur between 35 and 45 yrs of age , data on GLP-1RA suggests that could be benefit from exploring their use of in low grade PC patients on AS. Citation Format: Tim Oliver. Spontaneous Remission & Abscopal Responses in Prostate Cancer, a marker of “coldness”? [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Innovations in Prostate Cancer Research and Treatment; 2026 Jan 20-22; Philadelphia PA. Philadelphia (PA): AACR; Cancer Res 2026;86(2_Suppl):Abstract nr A051.

Background and ObjectivesLimbic-predominant age-related TDP-43 encephalopathy (LATE) is a neurodegenerative condition often overlapping clinically with Alzheimer disease (AD). No established in vivo biomarkers exist for LATE. The amygdalar atrophy scale (AAS) is a visual MRI rating tool scoring the amygdala as AAS0 (no atrophy), AAS1 (mild-to-moderate atrophy), or AAS2 (severe atrophy) and is associated with TDP-43 neuropathology in limbic regions. This study describes the clinical, neuroimaging, and longitudinal cognitive profiles of individuals classified using a proposed framework that combines the AAS with established AD biomarkers.MethodsThis retrospective study included individuals attending the Geneva Memory Center (2014–2022) who underwent T1-weighted MRI, as well as clinical and neuropsychological assessments. Participants were categorized with an etiologic grouping defined as No-AD/No-LATE (AAS0, negative AD biomarkers), AD (AAS0, positive AD biomarkers), LATE (AAS1–2, negative AD biomarkers), or AD/LATE (AAS1–2, positive AD biomarkers). Group differences were compared using Kruskal-Wallis or χ2 tests. Differences in MRI brain volumes and cortical thickness between groups were examined with analysis of covariance. Cognitive trajectories using Mini-Mental State Examination (MMSE) scores over 30 months were estimated with linear mixed-effects models accounting for baseline age and education.ResultsThe analytic sample included 469 participants (mean age 71.2 ± 8.5 years, 53% female). The No-AD/No-LATE group exhibited the highest MMSE scores (N = 181, 27.9 ± 2.2), outperforming AD (N = 146, 24.2 ± 4.9), LATE (N = 36, 26.2 ± 3.2), and AD/LATE (N = 106, 22.5 ± 5.3) groups (p < 0.001). On the Free and Cued Selective Reminding Test, the No-AD/No-LATE group showed the highest scores (15.1 ± 1.8); the LATE and AD groups performed similarly (13.3 ± 3.5 and 12.5 ± 4.0), both exceeding the AD/LATE group (10.6 ± 4.1) (p < 0.001). LATE and AD/LATE groups showed lower volumes/thicknesses in TDP-43–related regions compared with AD and No-AD/No-LATE groups. Longitudinally, the LATE group maintained cognitive stability as the No-AD/No-LATE group (β = −0.010, 95% CI −0.096 to 0.075, p = 0.813), whereas both AD (β = −0.136, 95% CI −0.184 to −0.088, p < 0.001) and AD/LATE (β = −0.139, 95% CI −0.196 to −0.082, p < 0.001) groups showed faster decline over time.DiscussionPatients identified as LATE by the integration of AAS with AD biomarkers had generally mild amnestic cognitive impairment, significant limbic atrophy, and slow decline over time, all features consistent with previous autopsy series. Moreover, AD/LATE cases were more impaired than those with LATE or AD alone. Prospective and neuropathologic validation is warranted.

The lifetime risk of stroke for adults of 25 years of age or older is approximately 25%, while stroke constitutes the second most common cause of mortality and the second most common cause of disability worldwide. In addition to the clinically manifest acute ischaemic stroke, the presence of cerebral infarction in patients without apparent clinical symptoms and signs attributed to ischaemic stroke or transient ischaemic attack was first described by Fisher in a series of autopsies. Over the years, the term 'silent brain infarction' has been replaced by the term 'covert cerebrovascular disease' (CCD).Despite the well-established evidence surrounding the associated sequelae of CCD, the current diagnostic and therapeutic algorithms in this particular group of patients are not well defined. With this case series, we showcase potential aetiologies and the value of individualised work-up and treatment strategies.

BackgroundPopulation aging is expected to increase the burden of Alzheimer's disease (AD) and related dementias (ADRD), yet up to 45% of ADRD risk may be modified. Disparities in ADRD burden among Hispanic/Latino and Black/African Americans suggests that socioeconomic deprivation and medical comorbidities may influence AD risk. The relationship between these factors, symptomatic age of onset, and neuropathologic findings in AD remains unclear. This study aims to investigate these associations in an ethnoracially diverse, neuropathologically diagnosed AD case series. Understanding these risk factors may help develop more effective AD risk reduction strategies.MethodWe queried the Florida Autopsied Multi‐Ethnic (FLAME) cohort database for neuropathologically‐diagnosed AD cases with available age onset of cognitive symptoms, who self‐identified as Hispanic/Latino (n = 75) or Black/African American (n = 22). Cases were matched to non‐Hispanic White decedents (n = 101) by sex and year of birth. Medical records at the time of brain donation were retrospectively reviewed, assessing completeness for demographics, clinical characteristics, and medical comorbidities (Table 1).ResultThe table shows a comparative analysis stratified by young‐onset AD (YOAD, onset <65 years) and late‐onset AD (LOAD, onset ≥65 years). YOAD cases had a significantly higher level of education compared to LOAD (p = 0.003). No differences were observed in sex, APOE ε4 carriership, or Area Deprivation Index between YOAD and LOAD. However, YOAD cases had a longer disease duration and were more likely to present with atypical clinical features compared to LOAD (both p <0.001). YOAD cases also showed a faster rate of decline on MMSE compared to LOAD (p = 0.002), higher frequency of depression (p = 0.018), and lower frequency of stroke/TIA (p = 0.025). YOAD cases also had lower brain weight (p = 0.041), less cerebrovascular disease burden (p = 0.003) and higher neurofibrillary tangle density in association cortices (p <0.001) compared to LOAD cases.ConclusionSocioeconomic deprivation and most medical comorbidities were not associated with AD symptomatic onset. Despite having higher education levels and lower cerebrovascular burden, YOAD decedents experienced faster cognitive decline but a longer disease course, with more frequent atypical clinical presentations and depression compared to LOAD. Further discussion will address the topographic distribution of tangle and plaque pathology.

Hepatocellular carcinoma, an underdiagnosed entity: An autopsy series.

Fungal infections in patients with haematological malignancies in the pre-triazole era: the dawn of a new era in medical mycology.

Hemothorax and needle thoracostomies in prehospital traumatic cardiac arrest: An autopsy series of 172 cases.

Methyl alcohol is a substance often associated with toxic effects and fatalities due to its use in the production of counterfeit alcohol. The primary mechanism of poisoning occurs when it is metabolized in the body by the enzyme alcohol dehydrogenase, resulting in the formation of formic acid. This formic acid can lead to metabolic acidosis, loss of vision, and neurological damage because of its strong toxic effects. Symptoms of poisoning may include vomiting, headache, cyanosis, and "blizzard vision." In such cases, the typical cause of death is acidosis, and the formation of formic acid can be mitigated by using ethyl alcohol as treatment. In forensic autopsies, the cause of death resulting from methanol poisoning, the method of ingestion, and the quantity consumed are determined through toxicological analysis. This study presents four cases of death due to methanol poisoning from the Artvin Forensic Medicine Branch Directorate and emphasizes the need to raise awareness, develop effective public health policies, and implement comprehensive measures to protect public health.

Although isolated ductus arteriosus aneurysm has been reported as 0.8% in autopsy series, it has recently been reported as up to 8.8% with increased awareness. Most cases are asymptomatic and regress spontaneously. In this study, we aimed to evaluate the characteristics, clinical manifestations, and outcomes of ductus arteriosus aneurysm in neonates. A total of 22 newborns with echocardiographic images recorded in the hospital registry system were identified to have a ductus arteriosus aneurysm. The demographic, clinical, and echocardiographic findings of the patients were extracted from the hospital records. The mean gestational age and weight at birth of the newborns were 38 6/7 weeks (35 3/7 - 40 6/7 weeks) and 3203 g (2445-4080 g), respectively. The maximal length and width of the aneurysm ranged from 6 to 21 mm and 5.3 to 13 mm, respectively. In three of the patients, thrombus in the aneurysm was detected on the third day of life, leading to surgical excision of thrombus and ligation of the aneurysm in two. In the remaining 19 patients, the aneurysm regressed spontaneously and closed in an average of 5.3 days. With increased awareness and earlier and more frequent application of echocardiography in newborns, the diagnosis of ductus arteriosus aneurysm is being reported more frequently. The most common scenario is spontaneous regression, however, it should not be forgotten that it can lead to serious complications, as reported previously. In selected cases, surgical treatment may be an option to prevent more serious or late complications, though the indications for surgical intervention remain unclear.

Hypothermia-related deaths present significant diagnostic challenges due to non-specific and often inconsistent autopsy findings. This study investigated the histological and immunohistochemical alterations associated with primary and secondary hypothermia in an experimental Rattus norvegicus model, focusing on the effects of benzodiazepine and alcohol ingestion. Twenty-one male rats were divided into three groups: control (K), benzodiazepine-treated (B), and alcohol-treated (A). After two weeks of substance administration, hypothermia was induced and multiple organ samples were analyzed. Histologically, renal tissue showed hydropic and vacuolar degeneration, congestion, and acute tubular injury across all groups, with no significant differences in E-cadherin expression. Lung samples revealed congestion, emphysema, and hemorrhage, with more pronounced vascular congestion in the alcohol and benzodiazepine groups. Cardiac tissue exhibited vacuolar degeneration and protein denaturation, particularly in substance-exposed animals. The spleen showed preserved architecture but increased erythrocyte infiltration and significantly elevated myeloperoxidase (MPO)-positive granulocytes in the intoxicated groups. Liver samples demonstrated congestion, focal necrosis, and subcapsular hemorrhage, especially in the alcohol group. Immunohistochemical analysis revealed statistically significant differences in MPO expression in both lung and spleen tissues, with the highest levels observed in the benzodiazepine group. Similarly, CK7 and CK20 expression in the gastroesophageal junction was significantly elevated in both alcohol- and benzodiazepine-treated animals compared to the controls. In contrast, E-cadherin expression in the kidney did not differ significantly among the groups. These findings suggest that specific histological and immunohistochemical patterns, particularly involving pulmonary, cardiac, hepatic, and splenic tissues, may help differentiate primary hypothermia from substance-related secondary hypothermia. The study underscores the value of integrating toxicological, histological, and molecular analyses to enhance the forensic assessment of hypothermia-related fatalities. Future research should aim to validate these markers in human autopsy series and explore additional molecular indicators to refine diagnostic accuracy in forensic pathology.

Contemporary medical literature indicates that metastases to the thyroid gland are relatively rare despite its rich vascular supply, accounting for approximately 1–3% of all malignant thyroid tumors. However, autopsy series studies demonstrate that metastases in the thyroid gland can be found in up to 24% of patients with advanced malignant disease.Objective. To examine a clinical case of a patient with papillary thyroid carcinoma.A clinical case was reviewed: Patient M., 75 years old, presented with a multinodular goiter.Results and Discussion: At the time of presentation, thyroid hormone levels were consistent with a euthyroid state. The patient complained of the presence of thyroid nodules and a sensation of discomfort. His medical history included previous surgical interventions: 25 years ago – left nephrectomy and splenectomy due to a renal neoplasm (discharge summaries not available); 10 years ago – prostatectomy and orchiectomy due to a malignant prostate tumor (no documentation provided). Laboratory parameters were within normal limits.Based on the medical history, physical examination, and ultrasound findings, a diagnosis of multinodular euthyroid goiter was established.A planned thyroidectomy was performed. No suspicion of malignancy was raised either prior to or during the surgical procedure.Histological Conclusion: Clear cell variant of papillary thyroid carcinoma.Oncologist's Conclusion: The treatment was carried out according to a radical protocol, and radioiodine therapy is not indicated for this patient. Replacement therapy with Euthyrox 100 mcg was prescribed.At follow-up visits, the patient's condition was satisfactory, with no complaints reported.Conclusion: Although metastases to the thyroid gland are rare, they should be considered in patients with a history of malignant tumors, particularly renal cell carcinoma.

Duodenal diverticular disease (DDD) is an uncommon condition of the gastrointestinal tract, with a reported prevalence of 0.2–5% in radiological studies and up to 22% in autopsy series. Although most cases are asymptomatic, complications such as bleeding, perforation, obstruction, or cholestasis may occur, requiring surgical intervention. Elective management is rare and should be individualized according to diverticulum location and symptom severity. This report presents a case of recurrent symptomatic DDD successfully managed with a duodenal switch technique. Surgical indications, therapeutic alternatives, and intraoperative findings are discussed within the context of the available literature. This approach represents a viable option in selected cases, enabling symptom resolution with a functionally favorable anatomical strategy.

Introduction: A large number of studies have been carried out for the etiology of atherosclerosis and many risk factors have been identified, including environmental factors and heavy metals, which are related to the pathogenesis. This study aimed to determine the effects of heavy metals, which have activation and inhibition effects on various metabolic pathways, on atherosclerosis by examining coronary arteries obtained from autopsy series. Methods: Coronary arteries of 28 autopsy cases were analyzed by inductively coupled plasma mass spectrometry method. Sixteen of the cases had coronary atherosclerotic plaques and 12 of the coronaries were normal. Twenty trace metal concentrations were examined from the samples obtained. Results: Twenty-eight coronary artery samples (16 with atherosclerosis, 12 normal) were analyzed using ICP-MS. Levels of Mg, K, Ca, P, Fe, Zn, Al, S, As, Pt, Sb, Hg were significantly higher in atherosclerotic arteries (e.g., Ca: 51,384 vs. 1,723 ppm, p = 0.005; P: 30,791 vs. 3,443 ppm, p = 0.003; Hg: 3.2 vs. 0 ppm, p < 0.001). Elements such as lead, cobalt, and cadmium remained below detection limits in both groups. Conclusion: Heavy metals through inflammation, oxidative stress, and disrupted antioxidant pathways are independent risk factors that increase the risk of atherosclerosis. These findings provide tissue-level evidence that heavy metal accumulation may contribute to atherosclerosis through oxidative stress, inflammation, and disruption of antioxidant defenses.

Foetal anomalies are congenital defects that can affect multiple organ systems, including the urogenital system. Congenital anomalies of the kidney and urinary tract (CAKUT) are a significant subset of these disorders, often leading to severe complications that impact foetal viability and affect postnatal outcomes. Early prenatal detection through imaging and genetic testing plays a crucial role in managing these conditions. Despite advances, foetal autopsy remains the gold standard for confirming diagnoses, identifying other associated anomalies, and understanding the embryological developmental basis of these defects. This autopsy series was conducted at the department of pathology, Sri Ramachandra institute of higher education and research, to analyse urogenital anomalies detected in foetal autopsies over a four-year period (January 2020-January 2024). Out of 352 foetal autopsies, 19 cases exhibited urogenital anomalies. We present a detailed analysis of five representative cases, which include unilateral renal agenesis associated with pentalogy of Cantrell, autosomal recessive polycystic kidney disease (ARPKD), Pearson syndrome with renal involvement, foetal megacystis, and bilateral renal agenesis with oligohydramnios (Potter syndrome). Each case highlights the complexity of urogenital malformations, their systemic implications, and the necessity for genetic counselling. These findings reinforce the importance of foetal autopsy in validating prenatal imaging and genetic results. Autopsy data provide valuable insights into the anatomical and pathological characteristics of these anomalies, aiding in the accurate classification of congenital disorders. Additionally, this series emphasises the role of genetic counselling in assisting parents with recurrence risk assessment and future planning. By integrating prenatal diagnostic techniques with post-mortem findings, this series emphasises the need for a multidisciplinary approach in managing congenital urogenital anomalies, thereby improving diagnostic accuracy, management, and family support strategies.

BackgroundAtrophic gastritis—the end stage of chronic gastritis—is an asymptomatic disease due to Helicobacter pylori infection causing decreased vitamin B12 and folate absorption, which may lead to severe haematological and neuropsychological disorders including Alzheimer’s disease. The diagnosis requires endoscopy and biopsies from symptomatic patients, explaining why its true prevalence in the population is not well-known.ObjectiveWe aimed to evaluate the prevalence of various stages of chronic gastritis in an autopsy series most closely representing the general population.Subjects and MethodsGastric mucosa samples were collected prospectively from out-of-hospital deaths included in the Tampere Sudden Death Study (n = 70, mean age 63, age range 22–91 years). Antrum and corpus samples were stained with a H. pylori antibody and staged histopathologically.ResultsChronic gastritis with or without atrophic changes was detected in 40% of the cases. The proportion of healthy mucosa decreased age-dependently from 71.4% among individuals aged <50 years to 43.5% among the oldest individuals (>70 years), and that of chronic non-atrophic gastritis from 21.4% to 8.7%. In contrast, the prevalence of atrophic gastritis was 27.1% and increased in the age groups from 7.1% to 47.8% (P = .019) among the oldest individuals, showing a strong association (P < .0001) with H. pylori immunopositivity.ConclusionsAtrophic gastritis is a common feature of the ageing stomach, which is observed in every second individual aged 70+ years, showing a strong association with H. pylori immunopositivity. Atrophic gastritis may be a more common risk factor in old age for diseases associated with low serum B12 and folate levels than has been previously known.

21 Respiratory Tract Localization of SARS-CoV-2 RNA in an Autopsy Series

Co-existing neuropathological comorbidities have been repeatedly reported to be extremely common in subjects dying with dementia due to Alzheimer disease. As these are likely to be additive to cognitive impairment, and may not be affected by molecularly-specific AD therapeutics, they may cause significant inter-individual response heterogeneity amongst subjects in AD clinical trials. Furthermore, while originally noted for the oldest old, recent reports have now documented high neuropathological comorbidity prevalences in younger old AD subjects, who are more likely to be included in clinical trials. Comorbid neuropathologies in subjects with Parkinson disease have received much less attention. As with AD, comorbidities may interfere with the evaluation of PD clinical trials. We have here examined the decadal-wise presence of multiple co-pathologies, and their clinical effects, in a series of autopsies of PD and control subjects from the Arizona Study of Aging and Neurodegenerative Disorders. Amyloid plaques were present in more than 40% of PD patients in their 60s, and in 85% of those in their 90s. Neurofibrillary tangles were present in PD, as in all elderly humans, from the 60s onwards, while Braak tangle stages of IV or greater, which are strongly associated with severe cognitive impairment, reached 40%, 50% and 60% in those subjects in their 70s, 80s and 90s, respectively. Both plaques and tangles were significant predictors of a lower MMSE score while greater CAA scores had borderline significance. None of these, however, were independently associated with a higher UPDRS score. The ApoE4 allele, while a known predictor of AD pathology, especially amyloid plaques, was not an independent predictor of function with either of these clinical measures, suggesting that its influence is largely mediated by the neuropathologies that it predisposes to. Non-AD tauopathies, including the major conditions of progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD), as well as the microscopic changes of argyrophilic grains (ARG) and aging-related tau astrogliopathy (ARTAG), also co-existed with PD, especially ARG and ARTAG, which ranged between 20% and 40% across decades for the former and up to 80% for the latter; we did not find significant associations of either with final MMSE or UPDRS scores. We failed to find a significant association of limbic TDP-43 histopathology with either final MMSE score or final UPDRS motor score but our subjects were more heavily weighted with PD than those in prior studies and our cognitive correlate, limited to MMSE score, may have missed associations with cognitive domain subsets. We found several cerebrovascular pathologies to be predictors of both cognitive and motor impairment, including brain infarcts, circle of Willis atherosclerosis, and higher white matter rarefaction score. All of the investigated pathology types were common in the non-demented, non-parkinsonian control subjects, and all increased with age in parallel with those co-existing with PD, while with generally lower prevalences. The high concurrence rate of the neurodegenerative protein aggregate diseases is suggestive of either a synergistic co-pathogenesis, where one aggregate type may instigate or accelerate another type, or of one or more underlying predisposing physiological or molecular mechanisms.

Sarcoidosis is a systemic granulomatous disease of unknown cause. The most commonly affected structures are the thoracic lymph nodes and the lungs, but any organ can be involved . In sarcoidosis, the heart can be affected both due to lung involvement and direct disease involvement. Clinically detected cardiac involvement is around 5%; However higher rates are reported in autopsy series. Endomyocardial biopsy, which is the definitive diagnostic method, is difficult and has low diagnostic value. Effective and reliable advanced cardiac imaging methods are needed in cardiac sarcoidosis . As well as the diagnosis of cardiac sarcoidosis, it is also important to determine disease activation, determine the treatment strategy, evaluate the severity, estimate the prognosis, and adjust steroid therapy . The most commonly used molecular imaging method in clinical practice for these purposes is Fluorodeoxyglucose (FDG) PET/CT imaging labeled with Fluorine-18 (F-18). Increased uptake in the myocardium on F-18 FDG PET/CT imaging is considered an important finding reflecting the activity of inflammation in cardiac sarcoidosis. In this report, two patients whose sarcoidosis diagnosis was confirmed histopathologically and who underwent PET CT examination due to cardiac sarcoidosis in our department are presented.

Objective: Patients with schizophrenia are at a higher risk of developing dementia, but the basis of cognitive impairment is a matter of discussion. Conflicting results regarding the association of schizophrenia with Alzheimer disease (AD) may partly be attributable to the inclusion of non-AD lesions, which few clinicopathological studies have considered. Therefore, a re-evaluation of an autopsy cohort of elderly schizophrenics published previously [1] was performed. Material & methods: Among 99 consecutive autopsy cases of patients who met the DSM-5 and ICD.10 criteria for schizophrenia (mean age 69.5 ± 8.25 years), 56 showed moderate to severe dementia. All brains were blindly examined using the current criteria for AD and looking for concomitant lesions. They were compared with the frequency of AD in an autopsy series of 1.750 aged demented individuals Results: Four cases revealed the features of definite AD, five probable AD, and three aged 82-89 years were classified as primary age-related tauopathy (PART). Two cases were a cortical type of dementia with Lewy bodies (DLB), one Lewy body disease of brainstem type; six showed hippocampal sclerosis, 14 argyrophilic grain disease (AGD), and one progressive supranuclear palsy (PSP). Other co-pathologies were frequent lacunes in basal ganglia, moderate cerebral amyloid angiopathy, minor development anomalies in the entorhinal cortex, Fahr's disease, metastatic tumors, and acute or old cerebral infarctions (n = 4 each). Definite AD was seen in 48 % of the age-matched demented control group. Conclusions: In this cohort of elderly schizophrenic patients, only 7.6 % fulfilled the neuropathological criteria of definite or probable AD and 3.6 % of PART compared to 6 % to 13.7 % typical and atypical AD in the literature, whereas a considerable number of cases showed non-AD co-pathologies. This is in line with other studies showing that the frequency of AD in elderly schizophrenics may be equal to or less than in age-matched controls. Further studies are needed to elucidate the mechanisms of cognitive decline in schizophrenia.