Basophilic invasion in the neurohypophysis is increased in patients with Alzheimer's disease.

PURPOSE: The prevalence of basophilic invasion (BI) and degenerative changes in the neurohypophysis of humans with neurodegenerative disease is not established. MATERIALS AND METHODS: We evaluated 122 pituitary glands reviewed at autopsy including 45 with Alzheimer's disease (AD) Braak and Braak stage V or VI, 18 with Lewy body disease (LBD), and 59 age-matched controls for BI. In addition, pituitary glands from 51 patients including 25 patients with AD and 18 aged-matched controls were studied with a periodic acid Schiff (PAS) stain and immunohistochemistry with a polyclonal antibody to nestin. Samples were graded as negative (0) or positive (1). RESULTS: BI was seen in 35 of 45 patients with AD (0.78 ± 0.06 mean and SE: 78%) and was significantly higher than 30 of 59 controls (0.51 ± 0.07; 51%) (p = 0.0236). BI was seen in 7 of 18 patients with LBD (0.39 ± 0.12; 39%) compared to controls (p = 0.387). BI was also significantly higher in AD compared to LBD (p = 0.0001). Nestin immunoreactivity was detected in the neurohypophysis of all patients. Definite nestin was not found in BI but was seen in Herring body-like structures, in pituicytes and axons. Phospho-τ-immunoreactive Herring bodies were seen in 65% with AD but phospho-τ-immunoreactive neurofibrillary tangles were not found. CONCLUSION: BI is increased in AD compared to controls or LBD but not associated with nestin immunoreactivity. The significance and role of BI as a marker for AD warrants additional study.

Basal Chronic Villitis and Disorders of the Placental Basal Plate: A Possible Immunological Link Between Hypertensive Disorders of Pregnancy and Morbidly Adherent Placenta.

BACKGROUND: Hypertensive disorders of pregnancy (HDP) are a common cause for preterm delivery. Prior studies showed that chronic villitis (CV) is associated with intrauterine growth restriction, preeclampsia, intrauterine fetal death, and morbidly adherent placenta (MAP). The authors hypothesize that disorders of the placental basal plate, especially basal chronic villitis (BCV), are associated with HDP. METHODS: The laboratory information system was queried over 12 years to identify placentas with or without the clinical history of HDP and with or without multifocal/focal CV or BCV. As a control for tissue sampling, a similar search was performed over 5 years for placentas evaluated for MAP. RESULTS: Of 19,683 placentas identified, 14.8% had CV which was in 18.5% and 14.2% of placentas associated with or without HDP, respectively, a significant difference (P < .0001). BCV was present in 6.0% and 3.9% of placentas with or without HDP, respectively, also a significant difference (P < .0001). BCV was more likely than multifocal/focal CV to occur in HDP (32.4% vs 27.4%) when all cases of CV were analyzed (P = .025). Of 221 placentas with MAP, 64% had multifocal/focal CV and 36% had BCV. CONCLUSIONS: BCV and CV are more common in placentas with HDP than in normotensive pregnancies. They are also seen in MAP, as supported by another recent study.