Indian journal of psychiatry
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Indian J Psychiatry · Jan 2010
Neuroanatomical correlates of psychopathology in antipsychotic-naïve schizophrenia.
Previous Magnetic Resonance Imaging (MRI) studies using manual techniques reporting significant relationship between psychopathology and gray matter volume in schizophrenia are limited by various confounding factors. None used automated image analysis to examine gray matter volume correlates of psychopathology in antipsychotic-naïve schizophrenia patients. ⋯ Cortical and cerebellar gray matter volume deficits and their significant negative correlations with psychopathology scores are supportive of 'Cognitive Dysmetria' in schizophrenia.
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The suicide rate in India is 10.3. In the last three decades, the suicide rate has increased by 43% but the male female ratio has been stable at 1.4 : 1. Majority (71%) of suicide in India are by persons below the age of 44 years which imposes a huge social, emotional and economic burden. ⋯ Physical and mental illness, disturbed interpersonal relationships and economic difficulties were the major reasons for suicide. The vulnerable population was found to be women, students, farmers etc. A social and public health response in addition to a mental health response is crucial to prevent suicidal behaviour in India.
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Alzheimer's disease (AD) is a devastating neurodegenerative disease, the most common among the dementing illnesses. The neuropathological hallmarks of AD include extracellular beta-amyloid (amyloid precursor protein (APP) deposits, intracellular neurofibrillary tangles (NFT)), dystrophic neuritis and amyloid angiopathy. The mismetabolism of APP and the defective clearance of beta amyloid generate a cascade of events including hyperphosphorylated tau (tau) mediated breakdown of microtubular assembly and resultant synaptic failure which results in AD. ⋯ 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.