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1.
J Alzheimers Dis ; 89(3): 769-788, 2022.
Article in English | MEDLINE | ID: mdl-35938246

ABSTRACT

BACKGROUND: As the Hispanic/Latino (HL) population grows, so too does the need for HL family caregivers for persons with dementia. HL caregivers tend to have less education, lower health literacy, and lower income, each uniquely compounding burden. Research is needed to appropriately tailor interventions for this population. OBJECTIVE: A systematic review and meta-analysis was conducted to 1) provide an updated review of non-pharmacologic intervention studies for HL dementia caregivers, 2) characterize promising interventions, and 3) highlight opportunities for future research. METHODS: Databases were searched for articles evaluating non-pharmacologic interventions for HL dementia caregivers. Studies were excluded if target populations did not include HLs or if no intervention was delivered. Data were extracted and random effects meta-analysis was performed on two primary outcomes: caregiver depression and burden. Effect sizes were calculated as pre- and post-intervention standardized mean differences (SMD), and further depression subgroup meta-analysis was performed. Other secondary outcome measures (e.g., perceived social support, caregiver knowledge, anxiety) were evaluated qualitatively. RESULTS: Twenty-three studies were identified. Most included multiple components pertaining to psychosocial support, caregiver education, and community resource facilitation. Many studies were successful in improving caregiver outcomes, though intervention design varied. Meta-analysis revealed minimal to moderate heterogeneity and small effect size in improving depressive symptoms (SMD = -0.31, 95% CI -0.46 to -0.16; I2 = 50.16%) and burden (SMD = -0.28, 95% CI -0.37 to -0.18; I2 = 11.06%). CONCLUSION: Although intervention components varied, many reported outcome improvements. Future studies may benefit from targeting physical health, addressing sociocultural and economic contexts of caregivers, and leveraging technology.


Subject(s)
Caregivers , Dementia , Anxiety , Caregivers/psychology , Dementia/psychology , Dementia/therapy , Hispanic or Latino , Humans , Psychosocial Support Systems , Quality of Life
2.
eNeuro ; 4(3)2017.
Article in English | MEDLINE | ID: mdl-28612047

ABSTRACT

Numerous studies have shown epilepsy-associated cognitive deficits, but less is known about the effects of one single generalized seizure. Recent studies demonstrate that a single, self-limited seizure can result in memory deficits and induces hyperactive phosphoinositide 3-kinase/Akt (protein kinase B)/mechanistic target of rapamycin (PI3K/Akt/mTOR) signaling. However, the effect of a single seizure on subcellular structures such as dendritic spines and the role of aberrant PI3K/Akt/mTOR signaling in these seizure-induced changes are unclear. Using the pentylenetetrazole (PTZ) model, we induced a single generalized seizure in rats and: (1) further characterized short- and long-term hippocampal and amygdala-dependent memory deficits, (2) evaluated whether there are changes in dendritic spines, and (3) determined whether inhibiting hyperactive PI3K/Akt/mTOR signaling rescued these alterations. Using the PI3K inhibitor wortmannin (Wort), we partially rescued short- and long-term memory deficits and altered spine morphology. These studies provide evidence that pathological PI3K/Akt/mTOR signaling plays a role in seizure-induced memory deficits as well as aberrant spine morphology.


Subject(s)
Androstadienes/therapeutic use , Dendritic Spines/drug effects , Memory Disorders/drug therapy , Memory Disorders/etiology , Protein Kinase Inhibitors/therapeutic use , Seizures/complications , Signal Transduction/drug effects , Animals , Animals, Newborn , Convulsants/toxicity , Dendritic Spines/ultrastructure , Disease Models, Animal , Enzyme Inhibitors/pharmacology , Fear , Female , Male , Pentylenetetrazole/toxicity , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Rats , Rats, Sprague-Dawley , Seizures/chemically induced , Seizures/pathology , Signal Transduction/physiology , Wortmannin
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