Bücher von Dileep Kumar

"The Leadership Blueprint: A Guide to Brilliance for Teens and Young Adults" is a guide designed to inspire, educate, and empower emerging leaders. The book draws from the author's years of experience mentoring young adults, offering invaluable insights into cultivating essential leadership skills like empathy, resilience, and innovation.Beyond the usual leadership rhetoric, the book delves into the unique challenges today's teens face and provides practical strategies to navigate this intricate journey. It also underscores the value of personal development, self-awareness, and introspection, building a foundation for effective leadership.From understanding the power of influence to the importance of creativity and innovation in problem-solving, this book offers comprehensive guidance for young leaders in the making. "The Leadership Blueprint" will inspire teens and young adults to step up and lead and equip them with the tools to make a significant difference in their worlds. This is an essential read for young minds ready to step into their leadership potential and leave a lasting impact.

This book explains the fundamental characteristics and biofunctionality of Alzheimer¿s Disease drug targets and provides up-to-date information on the full range of their biomedical applications. An introductory section gives an overview of the recent developments related to drug targets identified and studied related to Alzheimer¿s Disease and key developments from preclinical and clinical studies focusing on various molecular targets related to AD and dementia by subject experts all around the globe. Here, individual chapters address the progress and perspectives in human and non-human research, role of various biomarkers as an overview, advanced gene therapy, and novel compounds for therapeutic targets for Alzheimer¿s disease. The book will be essential reading for graduate students, scientists, and engineers in any of the biomedical research fields in which efforts are being made to utilize novel drug targets and develop effective strategies for new drug targeting and delivery in Alzheimer¿s disease treatment.

Self-development is a journey of personal growth and improvement. It's about becoming the best version of yourself and living a life that's fulfilling, purposeful, and meaningful. In this book, you will discover practical tips and strategies that will help you unlock your full potential and achieve your goals.You'll learn how to develop a growth mindset, overcome limiting beliefs, and cultivate positive habits. You'll also discover how to set clear and achievable goals, manage your time effectively, and deal with setbacks and challenges.The book will guide you through various aspects of self-development, including emotional intelligence, communication skills, and resilience. You'll gain insights into how to build strong relationships, handle stress, and maintain a positive outlook on life.With inspiring stories and actionable advice, this book will help you transform your life and achieve the success and happiness you desire. Whether you're looking to boost your career, improve your health, or enhance your relationships, this book will provide you with the tools you need to reach your full potential.

La enfermedad de Alzheimer (EA) es el tipo de demencia más común. Desde el punto de vista patológico, la EA se caracteriza por la presencia de placas amiloides y ovillos neurofibrilares en el cerebro, con la consiguiente pérdida de sinapsis y neuronas, lo que provoca déficits cognitivos y, finalmente, demencia. El péptido amiloide-¿ (A¿) y la proteína tau son los primeros componentes de las placas y los ovillos, respectivamente. En las décadas transcurridas desde que se identificaron A¿ y tau, el evento de las terapias para la EA se ha centrado principalmente en A¿, pero tau ha recibido más atención en los últimos años, en parte debido al fracaso de diversos tratamientos dirigidos a A¿ en los ensayos clínicos. Durante este artículo, revisamos el estado actual de las terapias dirigidas a tau para la EA. Dado que la patología de tau se correlaciona mejor con las alteraciones cognitivas que las lesiones de A¿, se espera que la focalización de tau sea más eficaz que la eliminación de A¿ una vez que los síntomas clínicos sean evidentes. Con las futuras mejoras en el diagnóstico, estos dos rasgos distintivos de la enfermedad podrían ser objeto de un tratamiento profiláctico.

Alzheimer's disease (AD), is a chronic neurodegenerative disease that causes senile decay of neurons It is the cause of 60¿70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. Genetic factors such as rare variants of TREM2(triggering receptor expressed on myeloid cells-2) strongly increase the risk of developing AD, confirming the role of microglia in AD pathogenesis. In the last 5 years, several studies have dissected the mechanisms by which TREM2, as well as its rare variants affect amyloid and tau pathologies and their consequences in both animal models and in human studies. In this review, we summarize increases in our understanding of the involvement of TREM2 and microglia in AD development that may open new therapeutic strategies targeting the immune system to influence AD pathogenesis.

La malattia di Alzheimer (AD) è il tipo più comune di demenza. Patologicamente, l'AD è caratterizzata da placche amiloidi e grovigli neurofibrillari nel cervello, con associata perdita di sinapsi e neuroni, portando a deficit cognitivi e infine alla demenza. Il peptide amiloide-¿ (A¿) e la proteina tau sono i primi componenti delle placche e dei grovigli, rispettivamente. Nei decenni da quando A¿ e tau sono stati identificati, l'evento di terapie per AD si è concentrato principalmente su A¿, ma tau ha ricevuto più attenzione negli ultimi anni, in parte a causa del fallimento di vari trattamenti A¿-targeting in studi clinici. In questo articolo, esaminiamo lo stato attuale delle terapie mirate alla tau per l'AD. Dato che la patologia tau si correla meglio con i deterioramenti cognitivi rispetto alle lesioni A¿, ci si aspetta che il targeting della tau sia più efficace della rimozione dell'A¿ una volta che i sintomi clinici sono evidenti. Con i futuri miglioramenti nella diagnostica, questi due segni distintivi della malattia potrebbero essere mirati in modo profilattico.

A doença de Alzheimer (AD) é o tipo mais comum de demência. Patologicamente, a DA é caracterizada por placas amilóides e emaranhados neurofibrilares dentro do cérebro, com perda associada de sinapses e neurônios, levando a déficits cognitivos e eventualmente demência. A amilóide¿ (A¿) peptídeo e a proteína tau são os primeiros componentes das placas e dos emaranhados, respectivamente. Dentro das décadas desde que o A¿ e a tau foram identificados, o evento das terapias para AD tem se concentrado principalmente no A¿, mas a tau tem recebido mais atenção nos últimos anos, em parte devido ao fracasso dos diversos tratamentos com o A¿ nos ensaios clínicos. Durante este artigo, revisamos o estado atual das terapias tau-targeting para a DA. Como a tau patologia se correlaciona melhor com as deficiências cognitivas do que as lesões do A¿, espera-se que o direcionamento da tau seja mais eficaz do que o clearance do A¿, uma vez que os sintomas clínicos são evidentes. Com futuras melhorias no diagnóstico, estas duas marcas da doença podem ser alvo de profilaxia.

La maladie d'Alzheimer (MA) est la forme la plus courante de démence. D'un point de vue pathologique, la MA se caractérise par la présence de plaques amyloïdes et d'enchevêtrements neurofibrillaires dans le cerveau, avec une perte associée de synapses et de neurones, entraînant des déficits cognitifs et finalement une démence. Le peptide amyloïde-¿ (A¿) et la protéine tau sont les premiers composants des plaques et des enchevêtrements, respectivement. Au cours des décennies qui ont suivi l'identification d'A¿ et de tau, les thérapies pour la MA se sont principalement concentrées sur A¿, mais tau a reçu plus d'attention ces dernières années, en partie à cause de l'échec de divers traitements ciblant A¿ dans les essais cliniques. Dans cet article, nous passons en revue l'état actuel des thérapies ciblant la protéine tau dans la MA. Étant donné que la pathologie tau est mieux corrélée avec les déficiences cognitives que les lésions A¿, le ciblage de la tau devrait être plus efficace que l'élimination de l'A¿ lorsque les symptômes cliniques sont évidents. Avec les améliorations futures des diagnostics, ces deux caractéristiques de la maladie pourraient être ciblées de manière prophylactique.

Alzheimer's disease (AD) is the commonest sort of dementia. Pathologically, AD is characterized by amyloid plaques and neurofibrillary tangles within the brain, with associated loss of synapses and neurons, leading to cognitive deficits and eventually dementia. Amyloid-¿ (A¿) peptide and tau protein are the first components of the plaques and tangles, respectively. Within the decades since A¿ and tau were identified, the event of therapies for AD has primarily focused on A¿, but tau has received more attention in recent years, partially due to the failure of varied A¿-targeting treatments in clinical trials. During this article, we review the present status of tau-targeting therapies for AD. Given that tau pathology correlates better with cognitive impairments than do A¿ lesions, targeting of tau is expected to give more effective than A¿ clearance once the clinical symptoms are evident. With future improvements in diagnostics, these two hallmarks of the disease might be targeted prophylactically.

Die Alzheimer-Krankheit (AD) ist die häufigste Form der Demenz. Pathologisch ist AD durch Amyloid-Plaques und neurofibrilläre Tangles innerhalb des Gehirns gekennzeichnet, mit einem damit verbundenen Verlust von Synapsen und Neuronen, was zu kognitiven Defiziten und schließlich zur Demenz führt. Amyloid-¿ (A¿)-Peptid und Tau-Protein sind die ersten Bestandteile der Plaques bzw. Tangles. In den Jahrzehnten seit der Identifizierung von A¿ und Tau hat sich das Geschehen der Therapien für AD hauptsächlich auf A¿ konzentriert, aber Tau hat in den letzten Jahren mehr Aufmerksamkeit erhalten, teilweise aufgrund des Scheiterns verschiedener A¿-zielender Behandlungen in klinischen Studien. In diesem Artikel geben wir einen Überblick über den derzeitigen Stand der Tau-gerichteten Therapien für AD. Da die Tau-Pathologie besser mit kognitiven Beeinträchtigungen korreliert als A¿-Läsionen, wird erwartet, dass ein Tau-Targeting effektiver ist als eine A¿-Beseitigung, sobald die klinischen Symptome offensichtlich sind. Mit zukünftigen Verbesserungen in der Diagnostik könnten diese beiden Kennzeichen der Krankheit prophylaktisch angegangen werden.