Alzheimer's disease (AD) is a devastating neurodegenerative disease, the most common among the dementing illnesses. The neuropathological hallmarks of AD include extracellular β-amyloid (amyloid precursor protein (APP) deposits, intracellular neurofibrillary tangles (NFT)), dystrophic neuritis and amyloid angiopathy. The mismetabolism of APP and the defective clearance of β amyloid generate a cascade of events including hyperphosphorylated tau (τ) mediated breakdown of microtubular assembly and resultant synaptic failure which results in AD. The exact aetiopathogenesis of AD is still obscure. The preeminent hypotheses of AD include amyloid cascade hypothesis and tau hyperphosphorylation. The amyloid hypothesis states that extracellular amyloid plaques formed by aggregates of Aβ peptide generated by the proteolytic cleavages of APP are central to AD pathology. Intracellular assembly states of the oligomeric and protofibrillar species may facilitate tau hyperphosphorylation, disruption of proteasome and mitochondria function, dysregulation of calcium homeostasis, synaptic failure, and cognitive dysfunction. The tau hypothesis states that excessive or abnormal phosphorylation of tau results in the transformation of normal adult tau into PHF-tau (paired helical filament) and NFTs. Vascular hypothesis is also proposed for AD and it concludes that advancing age and the presence of vascular risk factors create a Critically Attained Threshold of Cerebral Hypoperfusion (CATCH) which leads to cellular and subcellular pathology involving protein synthesis, development of plaques, inflammatory response, and synaptic damage leading to the manifestations of AD. Multiple other aetiological and pathogenetic hypotheses have been put forward including genetics, oxidative stress, dysfunctional calcium homeostasis, hormonal, inflammatory-immunologic, and cell cycle dysregulation with the resultant neurotransmitter dysfunctions and cognitive decline. The available therapeutic agents target only the neurotransmitter dysfunction in AD and agents specifically targeting the pathogenetic mechanisms like amyloid deposition and tau hyperphosphorylation might provide a definite therapeutic edge.

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Background: In addition to the socioeconomic problems, COVID-19 related lockdown may have profound mental health consequences. Aims and Objectives: The objectives were to assess the influence of lockdown on lifestyle, psychosocial stresses, and experienced quality of life (QOL). The study also assesses the association of the socio-demographic variables with lifestyle, psychosocial stress, and QOL. Methodology: An online survey on the lifestyle changes, psychosocial stress, and QOL were conducted using a validated questionnaire via the Google forms platform. The data collected were analysed using parametric and nonparametric tests. Results: The study included 263 respondents. The fear of developing COVID-19 was reported by 67.7%, 31.2% experienced weight gain, internet use was increased in 66.9%, and alcoholism and smoking decreased by 83.3% and 58.8%, respectively. Lockdown upset 48.3% moderately, and 36.1% experienced anxiety, 23.4% feared job loss, and 51.3% had financial worries. 91.1% of the study population reported fair to good QOL. Females showed significantly more religiosity, (Χ 2= 7.81; p= 0.02) did lesser exercise, (Χ 2= 10.9; p= 0.023) and had poor mood. (t=2.68; p=0.009) Older people were less afraid of COVID-19 infection and were less upset by the lockdown. The urban population was more fearful of COVID-19 and were more upset by the lockdown. Conclusion: Lockdown had a major effect on lifestyle and increased psychosocial stress, but people still experienced a fair QOL during this period.

Context:Psychological factors, such as that exist when we experience pain, can profoundly alter the strength of pain perception.Aim:The study aims to estimate the prevalence of psychiatric disorders, and its association with perception of pain and functional status in chronic patients in palliative care.Materials and Methods:The sample was selected via simple randomisation and post consent were assessed using (1) a semi- structured questionnaire to elicit socio-demographic information and medical data (2) Brief Pain Inventory (3) ICD-10 Symptom Checklist (4) ICD-10-Diagnostic Criteria for Research (DCR) (5) Montgomery Asberg Depression Rating Scale (MADRS) (6) Covi Anxiety Rating Scale (7) Karnofsky Performance Status Scale. Data was analysed using independent sample t test and chi square test.Results:The psychiatric morbidity was 67% with depression and adjustment disorders being the major diagnosis. There was a significant association between psychiatric morbidity pain variables (P = 0.000). Psychiatric morbidity significantly impaired activity, mood, working, walk, sleep, relationship, and enjoyment. There was no association between aetiology of pain, type of cancer, treatment for primary condition and treatment for pain and psychiatric morbidity. The functional status of cancer patients was also poorer in patients with psychiatric morbidity (P = 0.008).Conclusion:There is a high prevalence of psychiatric illness in chronic pain patients of any aetiology. Psychiatric morbidity is associated with increased pain perception, impairment in activity and poor functional status.