ABSTRACT
Objectives: Recent studies have shown that multilingualism may play an important role in enhancing cognitive health. The process of language acquisition constitutes a form of natural brain training, which in turn is hypothesized to increase neuroplasticity and hence, maintains the cognitive reserve. The study aimed to analyze the relationship between the number of languages known to an individual and its effect on cognitive functioning in both healthy and cognitively impaired study participants. Materials and Methods: This study utilized cross-sectional (baseline) data from Srinivasapura Aging, Neuro Senescence and COGnition study, which is an ongoing community-based, longitudinal aging cohort study conducted in a rural setting in southern India. A total of 3725 participants were considered for the study. The participants were separated into two groups, namely, monolinguals (participants knowing one language) and multilingual (participants knowing more than one language). The cognitive performance of the participants was assessed using the Clinical Dementia Rating (CDR) Scale. In addition, bivariate analyses and binary logistic regression analyses were carried out. Results: The result of CDR scores with respect to language category shows that, among the monolingual participants, 86.5% were healthy individuals and 13.5% were with mild cognitive impairment (MCI). Similarly, among the multilingual, 94.3% were healthy and 5.7% were with MCI. The odds ratio value derived from logistic regression (0.69 95% CI (0.5-0.9)) that an individual has a higher chance of developing cognitive impairment if he/she is a monolingual. Conclusion: This study highlights that knowing more than one language might have a profound positive impact on cognitive health, thereby reducing the likelihood of developing cognitive decline.
ABSTRACT
The growing prevalence of dementia makes it important for us to better understand its pathophysiology and treatment modalities, to improve the quality of life of patients and caregivers. Alzheimer's disease (AD), a neurodegenerative disease, is the most common form of amnestic dementia in the geriatric population. Pathophysiology of AD is widely attributed to aggregation of amyloid-beta (Aß) plaques and hyperphosphorylation of tau proteins. Initial treatment modalities aimed to increase brain perfusion in a non-specific manner. Subsequent therapy focused on rectifying neurotransmitter imbalance in the brain. Newer drugs modify the progression of the disease by acting against aggregated Aß plaques. However, not all drugs used in therapy of AD have been granted approval by the United States Food and Drug Administration (FDA). This review categorizes and summarizes the FDA-approved drugs in the treatment of AD in a manner that would make it a convenient reference for researchers and practicing physicians alike. Drugs that mitigate symptoms of dementia may be categorized into mitigators of Behavioral and Psychological Symptoms of Dementia (BPSD), and mitigators of cognitive decline. BPSD mitigators include brexpiprazole, an atypical antipsychotic with a once-daily dosage suited to treat agitation in dementia patients, and suvorexant, an orexin receptor antagonist used to treat sleep disturbances. Cognitive decline mitigators include cholinesterase inhibitors such as donepezil, rivastigmine, and galantamine and glutamate inhibitors such as memantine. Donepezil is the most commonly prescribed drug. It is cheap, well-tolerated, and may be prescribed orally once daily, or as a transdermal patch once weekly. It increases ACh levels, enhances oligodendrocyte differentiation and also protects against Aß toxicity. However, regular cardiac monitoring is required due to reports of cardiac conduction side effects. Rivastigmine requires a twice-daily oral dosage or once-daily replacement of transdermal patch. It has fewer cardiac side effects than donepezil, but local application-site reactions have been noted. Galantamine, in addition to improving cognitive symptoms in a short span of time, also delays the development of BPSDs and has minimal drug-drug interactions by virtue of having multiple metabolic pathways. However, cardiac conduction disturbances must be closely monitored for. Memantine, a glutamate regulator, acts as an anti-Parkinsonian agent and an antidepressant, in addition to improving cognition and neuroprotection, and requires a once-daily dosage in the form of immediate-release or sustained-release oral tablets. Disease-modifying drugs such as aducanumab and lecanemab reduce the Aß burden. Both act by binding with fibrillary conformations of Aß plaques in the brain. These drugs have a risk of causing amyloid-related imaging abnormalities, especially in persons with ApoE4 gene. Aducanumab is administered once every 4 weeks and lecanemab once every 2 weeks. The decision on the choice of the drug must be made after considering the availability of drug, compliance of patient (once-daily vs. multiple doses daily), cost, specific comorbidities, and the risk-benefit ratio for the particular patient. Other non-pharmacological treatment modalities must also be adopted to have a holistic approach toward the treatment of AD.
