Publications by authors named "Tali Benromano"

We studied whether there exist variations in pain responses between different intellectual and developmental disability (IDD) etiologies. Self-reports and facial expressions (Facial Action Coding System = FACS) were recorded during experimental pressure stimuli and compared among 31 individuals with IDD-13 with cerebral palsy (CP), nine with Down syndrome (DS), nine with unspecified origin (UIDD)-and among 15 typically developing controls (TDCs). The CP and DS groups had higher pain ratings and FACS scores compared to the UIDD and TDC groups, and steeper stimulus-response functions.

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Pain management necessitates assessment of pain; the gold standard being self-report. Among individuals with intellectual and developmental disabilities (IDD), self-report may be limited and therefore indirect methods for pain assessment are required. A new, internationally agreed upon and user-friendly observational tool was recently published-the Pain Assessment in Impaired Cognition (PAIC-15).

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Inhibition of insulin-degrading enzyme (IDE) is a possible target for treating diabetes. However, it has not yet evolved into a medical intervention, mainly because most developed inhibitors target the zinc in IDE's catalytic site, potentially causing toxicity to other essential metalloproteases. Since IDE is a cellular receptor for the varicella-zoster virus (VZV), we constructed a VZV-based inhibitor.

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Individuals with intellectual and developmental disabilities (IDD) are at a high risk of experiencing pain. Pain management requires assessment, a challenging mission considering the impaired communication skills in IDD. We analyzed subjective and objective responses following calibrated experimental stimuli to determine whether they can differentiate between painful and non-painful states, and adequately quantify pain among individuals with IDD.

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The present paper shows how cinnamon extract (CE) consumption mitigates neuronal loss and memory impairment following traumatic brain injury (TBI), one of the world's most common neurodegenerative diseases. TBI patients suffer short- and long-term behavioral, cognitive, and emotional impairments, including difficulties in concentration, memory loss, and depression. Research shows that CE application can mitigate cognitive and behavioral impairments in animal models for Alzheimer's and Parkinson's disease, whose pathophysiology is similar to that of TBI.

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Objective: Previous studies on the sensitivity and reactivity to pain of individuals with intellectual disability (ID) are inconsistent. The inconsistency may result from the reliance on self-reports and facial expressions of pain that are subject to internal and external biases. The aim was therefore to evaluate the reactivity to pain of individuals with ID by recording pain-evoked potentials (EPs), here for the first time, and testing their association with behavioral pain indices.

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Objective: As individuals with intellectual disability (ID) due to cerebral palsy (CP) are at high risk of experiencing pain, measuring their pain is crucial for adequate treatment. While verbal reports are the gold standard in pain measurements, they may not be sufficient in ID. The aim was to detect behavioral/autonomic responses that may indicate the presence and intensity of pain in individuals with CP and ID, using calibrated stimuli, here for the first time.

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Peripheral neuropathy is one of the main complications of diabetes mellitus. The current study demonstrated the bimodal pattern of diabetic peripheral neuropathy found in the behavioral study of pain perception in parallel to the histopathological findings in dorsal root ganglia (DRGs) neurons and satellite Schwann cell basement membranes. A gradual decrease in heparan sulfate content, with a reciprocal increase in deposited laminin in the basement membranes of dorsal root ganglia Schwann cells, was shown in streptozotocin-treated rats.

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Article Synopsis
  • - The study investigates how TGF-β1 influences insulin-degrading enzyme (IDE) activity, linking it to cerebrovascular amyloidosis (CA) and cognitive decline, particularly in Alzheimer's disease.
  • - Researchers found that TGF-β1 reduces IDE expression and activity in brain endothelial cells, leading to increased cerebrovascular pathology in mice lacking IDE compared to TGF-β1 only mice.
  • - Early reductions in synaptophysin protein levels in TGF-β1/IDE(-/-) mice suggest that TGF-β1 may contribute to cognitive impairment before significant age-related changes occur, highlighting potential therapeutic targets for cerebrovascular diseases.
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Article Synopsis
  • Cerebrovascular amyloidosis involves the buildup of amyloid in blood vessel walls, leading to issues like stroke and cognitive decline, particularly in Alzheimer's disease (AD).
  • Research shows that higher levels of TGF-β1 are linked to more amyloid deposition and are elevated near blood vessels in AD cases.
  • A study found that a nasally administered proteosome-based adjuvant can activate macrophages, reduce vascular amyloid, prevent brain damage, and enhance cognitive function in mice.
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An increasing body of evidence indicates that accumulation of soluble oligomeric assemblies of β-amyloid polypeptide (Aβ) play a key role in Alzheimer's disease (AD) pathology. Specifically, 56 kDa oligomeric species were shown to be correlated with impaired cognitive function in AD model mice. Several reports have documented the inhibition of Aβ plaque formation by compounds from natural sources.

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