Comparative effects of music interventions on depression in older adults: A systematic review and network meta-analysis.

Background: The effect of different music interventions on depression in older adults is varied. We aimed to explore the comparative effect of different music intervention features on depression in older adults. Methods: We searched PubMed, EMBASE, CENTRAL, CINAHL, and ProQuest Dissertations&Theses from inception to October 2021 for randomized controlled trials (RCTs) of music interventions in participants aged ≥60 years. Music interventions were classified based on the TIP (theme, intensity, and provider/platform) framework. The theme was divided into: 1) active music therapy (ACT); 2) receptive music therapy (Recep); and 3) music medicine (MM). The intensity was classified as high (>60 minutes/week), and low (≤60 minutes/week). The provider was classified as a music therapist (MT) or a non-music therapist (NonMT). Summary standardized mean differences (SMD) of level of depression with 95% confidence interval (CI) were estimated using a frequentist framework with a random-effects model. The certainty of evidence was evaluated using the Confidence in Network Meta-Analysis (CINeMA) approach. This study was registered with PROSPERO (CRD42021247165). Findings: Fifteen RCTs involving 1,144 older adults (mean age 67.9-86.6 years) were included. When compared with usual care, the most effective music intervention was active music therapy >60 minutes/week by music therapist (Act/High/MT) (SMD -3.00; 95%CI, -3.64,-2.35), followed by music medicine >60 minutes/week by non-music therapist (MM/High/NonMT) (SMD -2.06; 95%CI, -2.78,-1.35) with moderate and high certainty of evidence, respectively. Depression scores in older adults treated with ACT/High/MT was also significantly lower than all other interventions, except MM/High/NonMT. Low intensity music interventions other than Act/Low/MT had no impact on depression. Interpretation: Although active music therapy >60 minutes/week by music therapist is the most effective intervention to alleviate depression in older adults, music medicine by listening to music of older adult's own preference >60 minutes/week is an alternative approach in settings with limited resources. Funding: None.

Preventive effects of tamarind seed coat extract on UVA-induced alterations in human skin fibroblasts.

One of the most damaging actions on skin is from solar radiation, particularly from its ultraviolet (UV) component, through the formation of oxidative species. Thus, an antioxidant strategy that prevents the formation of these oxidants could form the basis of an efficacious cutaneous protectant. Many herbal materials contain antioxidant polyphenols, and this study assessed the possibility that tamarind seed coat extract could fulfill this role. An alcoholic extract of the tamarind (Tamarindus indica L.) seed coat showed stronger antioxidant activity (2,2-diphenyl-1-picrylhydrazyl inhibition, EC(50) = 12.9 µg/ml) than L-ascorbic acid (EC(50) = 22.9 µg/ml) and α-tocopherol (EC(50) = 29.3 µg/ml). In cultured fibroblasts taken from human skin, hydrogen peroxide (100-1000 µM) damaged 62-92% of the cells compared to only 35-47% when the cells were preincubated in extract (200 µg/ml) for 24 h. UVA (40 J/cm2) irradiation of human fibroblasts damaged 25% of the cells but the death rate was reduced to 10% with extract. UV irradiation increased the proportion of cells arrest in G(0)/G(1) phase (from 59% to 78%) but this was largely prevented by the extract (64%), according to flow cytometry. Intracellular total glutathione of UVA-irradiated cells pretreated with the extract increased to 10-25% compared to the non-pretreated group at 24-72 h after irradiation. Fibroblasts typically increased matrix metalloproteinase-1 secretion after photodamage, and this is prevented by the extract. This is the first report showing that tamarind seed coat extract is an antioxidant and can protect human skin fibroblasts from cellular damage produced by UVA and thus may form the foundation for an antiaging cosmetic.

Muscarinic M2 and M4 receptors in anterior cingulate cortex: relation to neuropsychiatric symptoms in dementia with Lewy bodies.

Alterations in cholinergic functions have been reported to be associated with neuropsychiatric symptoms in dementia. Increased M1 muscarinic receptor binding in temporal cortex is associated with delusions in dementia with Lewy bodies (DLB) patients and increased M2/M4 receptor binding with psychosis in Alzheimer's disease. However, the relation between M2 and M4 muscarinic receptor and psychotic symptoms in DLB is unknown. The aim of this study was to measure M2 and M4 receptors in the anterior cingulate cortex in DLB and to correlate the neurochemical findings with neuropsychiatric symptoms. Muscarinic M2 and M4 receptor levels in the anterior cingulate cortex and adjacent cortex (Brodmann's area [BA] 32) were measured separately by using a radioligand binding protocol based on binding of [(3)H]AF-DX 384 in the presence and absence of dicyclomine, a potent M4 receptor antagonist. M2 receptor binding was significantly increased, while M4 receptor binding was unchanged in the cingulate cortex and BA32 of DLB patients compared with age-matched controls. Impaired consciousness was significantly associated with increased M4 binding and delusions were significantly associated with increased M2 binding. Increased M2 and M4 receptor binding in DLB was also associated with visual hallucinations. Upregulation of M2 and M4 muscarinic receptors in cingulate and adjacent cortex may thus contribute to the development of psychosis in DLB, with potential implications for treatments with drugs acting on these receptors.

Nicotinic acetylcholine receptor immunohistochemistry in Alzheimer's disease and dementia with Lewy bodies: differential neuronal and astroglial pathology.

Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are common forms of dementia in the elderly. The neuropathology of AD and DLB is related to cholinergic dysfunctions, and both alpha4 and alpha7 nicotinic acetylcholine receptor (nAChR) subunits are decreased in several brain areas in both diseases. In this immunohistochemical study, we compared neuronal and astroglial alpha4 and alpha7 subunits in AD, DLB and age-matched controls in the hippocampal formation. The numbers of alpha4 reactive neurons were decreased in layer 3 of the entorhinal cortex of AD and DLB, whereas those of alpha7 reactive neurons were decreased in layer 2 of the subiculum of AD and DLB and in layer 3 of the entorhinal cortex of DLB. In contrast, the intensity of alpha7 reactive neuropil was significantly higher in AD than in controls or DLB in a number of areas of the hippocampus (CA3/4 and stratum granulosum), subiculum and entorhinal cortex. An increase in alpha7 immunoreactivity in AD was also associated with astrocytes. The number of astrocytes double-labelled with alpha7 and glial fibrillary acidic protein (GFAP) antibodies was increased in most areas of the hippocampus and entorhinal cortex in AD compared with controls and DLB. Increased astrocyte alpha7 nAChRs in AD may be associated with inflammatory mechanisms related to degenerative processes specific to this disease.

Alzheimer's disease is associated with a selective increase in alpha7 nicotinic acetylcholine receptor immunoreactivity in astrocytes.

Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are common forms of dementia in the elderly associated with cholinergic dysfunction, including reductions in nicotinic acetylcholine receptors (nAChRs). In AD, astrocytes are implicated in the formation of senile plaques, one of the core pathological features. Using immunohistochemistry, we have investigated astrocytic expression of the two major nicotinic receptor alpha subunits in the human hippocampus and entorhinal cortex. alpha7, but not alpha4, subunit immunoreactivity was associated with astrocytes. An increase in the proportion of astrocytes expressing alpha7 immunoreactivity was observed in AD compared with age-matched controls. A similar increase was not evident in DLB. Elevated alpha7 nAChRs on astrocytes in AD may contribute to alterations in calcium homeostasis and nitric oxide production, which in turn could affect beta-amyloid-mediated inflammatory processes in AD.