Knowing what to expect can help everyone prepare for what is coming, and knowing about what support and services are available is key to living well with dementia. These books are a comprehensive resource specifically tailored for a New Zealand audience. They are based on the latest insights and research, and we hope you find them useful. A few printed booklets are available from your local Alzheimers organisation. The booklet provides information on what dementia is, as well as the early warning signs and how to go about getting a diagnosis. It also explains what support is available and the things you can do to prepare for the future.
Click here to download the booklet PDF. Living well with dementia A guide for people diagnosed with dementia This booklet is written for people who have been diagnosed with dementia to give you information and to help you continue to live well. The booklet suggests ways to look after yourself including how to adjust to change and managing your day, as well as working, driving, keeping involved and active and planning for the future. This booklet gives you information and tips on helping a person with dementia with their personal care, such as washing and dressing, nutrition, sleeping and travelling, as well as communication and ideas for meaningful activities and ways you can look after yourself — which is very important, too.
It includes information about what might be causing the behaviour and some tips to help you support the person with dementia to live well. By necessity, this booklet contains clinical terminology and is structured so you can easily find a certain situation such as agitation or hallucinations. This resource is designed to provide information about transitioning from home to residential care. The booklet provides information on topics such as deciding on residential care, what to look for when choosing a care facility, and how to cope when the person you have been caring for goes into residential care.
This booklet is designed to provide information about what to expect in the last stage of dementia. It highlights some issues that may be useful to consider, including what happens as the end of life nears and after death has occurred. These sheets are available in PDF format for you to download and read or print out. To read the pdfs you will need Acrobat Reader, which most computers already have installed. Click on the links below to view the factsheets. Some of the people shown in photographs on the Alzheimers NZ website and social media channels are stock photography models.follow
Alzheimer’s and Dementia Behavior Management - yxogakifod.cf
Copyright Site by Kudos Web. Alzheimers New Zealand For dementia support call According to the World Health Organization WHO , caring for and treating people with dementia currently costs the world more than billion dollars per year. Alzheimer's disease is the most frequent cause of dementia and has become a major public health concern; in fact the WHO declared dementia a public health priority.
As a previous State Secretary of Research and Education in Switzerland, I am aware of the challenge to governments and health systems, but also to families to care for the growing number of patients suffering from Alzheimer's disease. Finding a cure for this devastating disease is top priority. Many research organizations, thousands of research laboratories and hospitals, various biotech and pharma companies, patient organizations, and foundations have devoted enormous efforts to find therapeutic agents to cure or prevent this terrible disease, with few and disappointing results.
Neurodegenerative diseases are so daunting that the most important—and rare—ingredient today is courage to follow new ideas, untrodden paths, and disruptive innovations. As a trained neurologist, psychiatrist, and neuropathologist, Dr. Judith Miklossy has early on detected that spirochetes helically shaped bacteria when they invade brain cells, reproduce the filamentous pathology characteristic of Alzheimer's disease. Judith Miklossy has defended nearly single-handedly the hypothesis that chronic infection by spirochetes and several other important pathogens could constitute risk factors for Alzheimer's disease.
This is still a debated and largely underfunded alley of research in Alzheimer's disease. But if this hypothesis holds true, early intervention against infection may delay or even prevent the future development of Alzheimer's disease. As a former State Secretary responsible for science policy, I always wondered how we could foster disruptive, innovative research. Granting agencies, with a well-established and necessary peer-review cycle, have trouble funding research for new disruptive ideas.
Personalities like Judith, and foundations like the Prevention Alzheimer International Foundation established in Switzerland are the engines of this necessary type of research.
Alzheimer's disease is too important and tragic for us to neglect any promising avenue. Two basic discoveries spurred research into inflammation as a driving force in the pathogenesis of Alzheimer's disease AD. The first was the identification of activated microglia in association with the lesions. The second was the discovery that rheumatoid arthritics, who regularly consume anti-inflammatory agents, were relatively spared from the disease. These findings led to an exploration of the inflammatory pathways that were involved in AD pathogenesis.
This focused attention on anti-inflammatories as blockers of complement activation. A consistent finding has been that the longer the NSAIDs were used prior to clinical diagnosis, the greater the sparing effect. They have established that the onset of AD commences at least a decade before cognitive decline permits clinical diagnosis.
Such biomarker studies have revealed that a huge window of opportunity exists when application of NSAIDs, other anti-inflammatory agents, or complement activation blockers, could arrest further progress of AD, thus eliminating its manifestation. It can be anticipated that this principle will apply to many other chronic neurodegenerative diseases.
HEAD TRAUMA LINKS TO DEMENTIA
Neuroinflammation, discovered in AD more than 30 years ago, has now become a major field of brain research today. Inhibiting it may be the key to successful treatment of many chronic neurological disorders.
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They assemble in response to cellular infection and stress or to tissue damage, promote inflammatory reactions, and are important in regulating innate immunity particularly by acting as platforms for activation of caspase proteases. They appear to be involved in several pathological processes activated by microbes including Alzheimer's disease AD.
Best characterized in microbial pathogenesis is the nucleotide-binding domain and leucine-rich repeat NLR -protein 3 NLRP3 inflammasome.
For decades, the role of the innate immune system in the etiology of AD was considered less important, but the recently discovered inflammatory genes by genome-wide association studies driving inflammation in this disease has changed this view. The weak immunostimulatory activity is a consequence of their immune evasion strategies and survival. In addition, we discuss the plausible contribution of specific bacteria playing a role in influencing the activity of the NLRP3 inflammasome to AD progression.
Alzheimer and a number of other neurodegenerative diseases are characterized by the presence of reactive microglia and reactive astrocytes in association with the lesions. The classic view that microglia exist primarily in either a resting or activated state needs to be broadened in view of recent results.
Resting microglia are in constant activity sampling their surround. Activated microglia may be pro-inflammatory, releasing inflammatory cytokines and other inflammatory mediators, or anti-inflammatory, promoting the healing process. There is evidence that microglial phagocytosis is more powerful in the anti-inflammatory state. Activated astrocytes also have pro-inflammatory and anti-inflammatory properties. In the pro-inflammatory state they release inflammatory cytokines. In the anti-inflammatory state they release various growth factors.
In AD and other neurodegenerative diseases, both microglia and astrocytes are in a pro-inflammatory state. From a therapeutic point of view it is desirable to find methods of tipping the balance towards an anti-inflammatory state for both types of glia. Sporadic, late-onset Alzheimer's disease LOAD is a progressive neurodegenerative disease that is now the most common and severe form of dementia in the elderly. That dementia is thought to be a direct result of neuronal damage and loss associated with accumulations of abnormal protein deposits in the brain.
The neuropathology observed includes: neuritic senile plaques NSPs , neurofibrillary tangles NFTs , neuropil threads NPs , and often deposits of cerebrovascular amyloid. However, a number of recent and ongoing studies have implicated infection in the etiology and pathogenesis of LOAD. Chronic bacterial infections are frequently associated with amyloid deposition. It had been known from a century that the spirochete Treponema pallidum can cause dementia in the atrophic form of general paresis where.
It is noteworthy that the pathological hallmarks of this atrophic form are similar to those of AD. Bacteria or their poorly degradable debris are powerful inflammatory cytokine inducers, activate complement, affect vascular permeability, generate nitric oxide and free radicals, induce apoptosis and are amyloidogenic. All these processes are involved in the pathogenesis of AD.
Old and new observations, reviewed here, indicate that to consider the possibility that bacteria, including several types of spirochetes highly prevalent in the population at large or their persisting debris may initiate cascade of events leading to chronic inflammation and amyloid deposition in AD is important, as appropriate antibacterial and antiinflammatory therapy would be available to prevent dementia. The cause, or causes, of the vast majority of Alzheimer's disease cases are unknown.
A number of contributing factors have been postulated, including infection. It has long been known that the spirochete Treponema pallidum, which is the infective agent for syphilis, can in its late stages cause dementia, chronic inflammation, cortical atrophy and amyloid deposition. Spirochetes of unidentified types and strains have previously been observed in the blood, CSF and brain of 14 AD patients tested and absent in 13 controls.
In three of these AD cases spirochetes were grown in a medium selective for Borrelia burgdorferi. In the present study, the phylogenetic analysis of these spirochetes was made. Positive identification of the agent as Borrelia burgdorferi sensu stricto was based on genetic and molecular analyses. Borrelia antigens and genes were co-localized with beta-amyloid deposits in these AD cases.
The data indicate that Borrelia burgdorferi may persist in the brain and be associated with amyloid plaques in AD. They suggest that these spirochetes, perhaps in an analogous fashion to Treponema pallidum, may contribute to dementia, cortical atrophy and amyloid deposition. Further in vitro and in vivo studies may bring more insight into the potential role of spirochetes in AD. Here we show there is no statistically significant correlation between the incidence of LD and deaths due to AD in the US.
Recent work by several other research groups has validated this conclusion. Alzheimer's disease AD is an infectious disease caused by spirochetes,and these spirochetes form biofilms, which attract the innate immune system. NOTE: By entering your email address you confirm that you have read and agree to our terms and conditions.
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