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What a beautiful morning
Every morning is beautiful when Noah visits his Grandparents. When Grandpa and Noah wake up, they take off singing and hardly stop: walking the dog, splashing through puddles, and eating French toast with cinnamon. But one summer Grandpa seems to have forgotten how to do the things they love. Does he even know who Noah is? Grandma steps in energetically, filling in as best she can. But it is Noah who finds the way back to something he can share with Grandpa. Something musical. Something that makes the morning beautiful again. This is a story about how love helps us find even what we think is lost.
Book
Unforgotten
As life expectancy increases in India, the number of people living with dementia will also rise. Yet little is known about how people in India cope with dementia, how relationships and identities change through illness and loss.
eBook
The 36-hour day : a family guide to caring for people who have Alzheimer disease, related dementias, and memory loss
Provides practical and legal advice on caring for those who can no longer care for themselves, including information on dealing with such daily problems as eating and exercising, and suggests ways to cope with mood swings and false ideas.
Book
The fragile brain : the strange, hopeful science of dementia
In Fragile Brains Kathleen Taylor looks at the genetic and lifestyle factors currently linked to the development of dementia, focusing on important new research on how the immune system operates in the brain.
eBook
Non-Alzheimer's and Atypical Dementia
Dementia is the most common type of neurodegenerative disorder. Non-Alzheimer's and Atypical Dementia concentrates on each form of dementia individually, considering symptoms, diagnosis and treatment
* Focuses on non-Atypical Dementia
* Multidisciplinary approach to diagnosis and management
* Allows development of management and care plan strategies
* Practical approach including case studies
* Written by a world-renowned editorial team
eBook
Just Lucky
When her grandfather dies and her grandmother is diagnosed with dementia, fifteen-year-old Lucky must navigate the foster-care system.
Book
lost in space
Dementia presents immense challenges - both for individuals as well as for society as a whole. More than 35 million people all over the world currently live with dementia, a number that is expected to double by 2050. This also has implications for architecture and urban planning because dementia often affects people's sense of orientation and their ability to perceive space. How can homes, apartments, public buildings, outdoor spaces, neighbourhoods and cities, as well as environments and infrastructure, be designed to meet the needs of people with dementia as well as those of their caregivers? And can a consideration of the problems of dementia lead to a better understanding of space that can improve architecture and the built environment for us all? This book addresses these and other questions in a series of professional essays that examine the specific requirements for different disciplines. In addition, international case study projects illustrate the breadth of current actual solutions. The book is intended as a guide for all those involved in the design and planning process - architects, interior designers, engineers, town planners, local authorities and clients - and as a reader for the users themselves: for people with dementia, their family and friends, and all those in their social environment.
eBook
Exercise suppresses neuroinflammation for alleviating Alzheimer’s disease
Alzheimer’s disease (AD) is a chronic neurodegenerative disease, with the characteristics of neurofibrillary tangle (NFT) and senile plaque (SP) formation. Although great progresses have been made in clinical trials based on relevant hypotheses, these studies are also accompanied by the emergence of toxic and side effects, and it is an urgent task to explore the underlying mechanisms for the benefits to prevent and treat AD. Herein, based on animal experiments and a few clinical trials, neuroinflammation in AD is characterized by long-term activation of pro-inflammatory microglia and the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasomes. Damaged signals from the periphery and within the brain continuously activate microglia, thus resulting in a constant source of inflammatory responses. The long-term chronic inflammatory response also exacerbates endoplasmic reticulum oxidative stress in microglia, which triggers microglia-dependent immune responses, ultimately leading to the occurrence and deterioration of AD. In this review, we systematically summarized and sorted out that exercise ameliorates AD by directly and indirectly regulating immune response of the central nervous system and promoting hippocampal neurogenesis to provide a new direction for exploring the neuroinflammation activity in AD.
Journal Article
Autophagy–lysosomal-associated neuronal death in neurodegenerative disease
Autophagy, the major lysosomal pathway for degrading damaged or obsolete constituents, protects neurons by eliminating toxic organelles and peptides, restoring nutrient and energy homeostasis, and inhibiting apoptosis. These functions are especially vital in neurons, which are postmitotic and must survive for many decades while confronting mounting challenges of cell aging. Autophagy failure, especially related to the declining lysosomal (“phagy”) functions, heightens the neuron’s vulnerability to genetic and environmental factors underlying Alzheimer’s disease (AD) and other late-age onset neurodegenerative diseases. Components of the global autophagy–lysosomal pathway and the closely integrated endolysosomal system are increasingly implicated as primary targets of these disorders. In AD, an imbalance between heightened autophagy induction and diminished lysosomal function in highly vulnerable pyramidal neuron populations yields an intracellular lysosomal build-up of undegraded substrates, including APP-βCTF, an inhibitor of lysosomal acidification, and membrane-damaging Aβ peptide. In the most compromised of these neurons, β-amyloid accumulates intraneuronally in plaque-like aggregates that become extracellular senile plaques when these neurons die, reflecting an “inside-out” origin of amyloid plaques seen in human AD brain and in mouse models of AD pathology. In this review, the author describes the importance of lysosomal-dependent neuronal cell death in AD associated with uniquely extreme autophagy pathology (PANTHOS) which is described as triggered by lysosomal membrane permeability during the earliest “
intraneuronal
” stage of AD. Effectors of other cell death cascades, notably calcium-activated calpains and protein kinases, contribute to lysosomal injury that induces leakage of cathepsins and activation of additional death cascades. Subsequent events in AD, such as microglial invasion and neuroinflammation, induce further cytotoxicity. In major neurodegenerative disease models, neuronal death and ensuing neuropathologies are substantially remediable by reversing underlying primary lysosomal deficits, thus implicating lysosomal failure and autophagy dysfunction as primary triggers of lysosomal-dependent cell death and AD pathogenesis and as promising therapeutic targets.
Journal Article