Apolipoprotein E gene allele 4 (APOE4) is a major genetic risk factor for late-onset Alzheimer’s disease (AD). Individuals carrying one copy of the APOE4 allele are known to be at 3-4-fold increased risk of developing AD compared with those carrying the more common APOE3 allele.
Apolipoprotein E gene allele 4 (APOE4) is not only “genetic”. APOE-ε4 alleles are known to show a distinct increase in tuberculosis [Taghi Naserpour Farivar., et al. “Apolipoprotein E Polymorphism in Tuberculosis Patients”. Journal of Applied Sciences 8.4 (2008): 719-722], Thank you.
A transformation in our understanding of dementia is happening through advances in biomarkers, genetics, and other data used as dementia risk evidence (DRE) promising a future for precision dementia care.
The TSE’S or transmissible spongiform encephalopathies, include bovine spongiform encephalopathy (also called BSE or “mad cow disease”), Creutzfeldt–Jakob disease (CJD) in humans, and “scrapie” in sheep or goats (caprine spongiform encephalopathy). They remain a mystery, their cause still hotly debated. Current mad cow diagnosis lies solely in the detection of late appearing “prions”, an acronym for hypothesized, gene-less, misfolded proteins, somehow claimed to cause the disease. Yet laboratory preparations of prions contain other things, which could include unidentified bacteria or viruses. And the only real evidence that prion originator Stanley Prusiner had in his original paper that the disease agent behind “Scrapie” in sheep and goats was devoid of DNA or RNA– was based upon the fact that he couldn’t find any. Furthermore, the rigors of prion purification alone, might, in and of themselves, have killed any causative microorganism and Heino Dringer, who did pioneer work on their nature, candidly predicts “it will turn out that the prion concept is wrong.” Roels and Walravens as well as Hartly traced Mad Cow to Mycobacterium bovis. Moreover, epidemiologic maps of the origins and peak incidence of Mad Cow in the UK, suggestively match those of England’s areas of highest bovine tuberculosis, the Southwest. The neurotoxic potential of bovine tuberculosis has for some time been well known. By 1911 Alois Alzheimer called attention to “a characteristic condition of the cortical issue which Fischer referred to as ‘spongy cortical wasting” in Alzheimer’s disease (AD). But behind AD, Fischer suspected a microbe called Streptothrix which was constantly being mistaken and confused for tuberculosis. Our present investigation of the TSEs clearly shows cell-wall-deficient (CWD) tubercular mycobacteria present, verified by molecular analysis, ELISA, PCR and microscopy to cause spongiform encephalopathy.
Keywords: Prions; Scrapie; The Spongiform Encephalopathies; Alzheimer’s disease;The eiology of Alzheimer’s Disease; Mycobacterium tuberculosis Complex
The identification of Aβ peptides as the major components of amyloid plaque and the discovery in familial cases of Alzheimer’s diseases (AD) of multiple mutations in the genes implicated in their production led to the formalization of the Amyloid Hypothesis (AHyp) .
Sometimes social pressures come to a head, and a moment of crisis offers opportunity. With the disastrous FDA approval of aducanumab (or Aduhelm, as the drug is known in its commercial existence) in June, the figurative “boil” of the Alzheimer’s disease movement has done just that.
Amyloids are insoluble extracellular depositions of protein fibrils with a typical X-ray diffraction pattern. Amyloid fibrils are composed of polypeptide chains arranged in a twisted β-pleated sheet conformation.
One of the most jaw-dropping reversals of guidance procedures in the history of the FDA took place last June 7, when the agency announced that the drug aducanumab, a monoclonal antibody manufactured by Biogen and Eisai, biotech companies for the treatment of AD, had received marketing approval.
Risk factors for dementia are by now well established, with particular lifestyle factors/choices shown to have a significant impact on the development of dementia. However, much less is known in how much our environment potentially influences the risk for dementia.
Eugenia Zukerman, flute virtuoso, author and television music reporter, has clinical Alzheimer’s disease (AD). She has openly discussed her condition with the media, and wrote about it in her latest book, “Like Falling Through a Cloud: A Lyrical Memoir,” published late last year.
An exploratory study, conducted by NetNoggin®, revealed that among those impacted by Alzheimer's, hope of finding a cure is deflating due to recent clinical trial failures. This exploration was a combination of secondary analysis and primary netnographic research.
It is estimated that around 45 million people in the world suffer from dementia, most of them over 60 years old. With increases in life expectancy, this incidence is projected to double every 20 years .
In the last few years, we have witnessed a tremendous advancement in cell culturing methods. The scene has been dominated by the optimization of 3D in vitro models either in the form of dissociated neuronal cultures or of the so-called organoids.
Alzheimer's disease (AD) is the most prevalent form of dementia with large impact on population over the age of 65 years . The most distinctive symptomatic phase during the disease is the decline of the cognition with the loss of synapses [2-5].
This blog is a follow-up to the one I published in August 2017, titled “Music Experiences for Persons with AD”. In this piece, I am focusing on one of the experiences: Music Therapy. As an inexpensive, evidence-based, and non-pharmacological treatment, music therapy should highly be considered in the total care package for persons living with AD.
In Alzheimer’s disease (AD), we are gaining great ground in the field of early diagnosis, but disease-modifying drugs are still missing. While many studies have been focused on the pathogenic role of amyloid-β (Aβ) dysmetabolism, recent preclinical and clinical findings revealed a more complex picture. In AD, we need to embrace a complex view of the disease state as a condition resulting from the converging failure of health-controlling systems and networks; A condition shaped by the combination of our “omic” blueprint and the influence of the environment.
The search to find therapeutic targets in Alzheimer's disease (AD) has been dominated for over 25 years by research into the roles in the initiation and progression of dementia of the amyloid beta protein (Aβ) [1, 2], derived from the β-pathway of amyloid beta protein (AβPP) cleavage.
An ancient Indian subcontinent parable tells a story in which a group of blind men each touch a different part of an elephant. They cannot agree on the nature of the elephant because none of them observed the elephant as a whole.
Alois Alzheimer might have mentioned plaques and tangles in a single short paper on pre-senile dementia in 1907, but it was the co-discover of Alzheimer’s disease (AD), Oskar Fischer, who in that same year far more extensively reported neuritic plaque in 12 cases of senile dementia, a condition which he and many others refused to differentiate from Alzheimer’s “pre-senile” dementia.
Music is a wonderful, non-pharmacological intervention to be considered for persons with Alzheimer’s disease (AD). In order to provide appropriate and beneficial music interventions for persons with AD, it is important to understand the range of music experiences that may offer effective complementary management of symptoms associated with AD.
The World Health Organization  has declared dementia as public health priority. Alzheimer’s disease (AD) is the most frequent cause of dementia. The challenges to governments to respond to the growing number of people with dementia are substantial. Tremendous efforts have been made in research during the last four decades highlighting important aspects of the pathogenesis of AD, but if the cause of AD is not defined, and treatments to prevent the disease are not provided, the world will face an unprecedented health-care problem by the middle of the century.
There is increasing concern not only in Alzheimer’s disease (AD) research, but all of modern investigations, that false findings may be the majority or even the vast majority of published research claims .
Alzheimer’s disease (AD) is the most common cause of dementia and remains incurable. Its prevalence is rising, current afflicting 5 million Americans with projections to affect millions more as the population ages .
Among patients diagnosed with Alzheimer's disease (AD), the percentage in the severe stage ranges from 28%  to 33%  to a maximum of 50% . In institutionalized patients, prevalence is higher, with an estimated 75% of patients with severe AD .
There is no doubt that nutrition is involved in brain health and the development of neurodegenerative diseases. This is an important area of research in the dementia field that has suffered from the absence of trained experts in nutrition and nutritional epidemiology.
Most of us harbour in our body several types of herpes virus—perhaps as many as five—and we provide them with a safe and secluded haven for life, as there are no methods for eliminating or expelling them.
The ability to maintain normal psychological and physical functioning and avoid serious mental illness when exposed to stress and trauma, a phenomenon known as resilience, is a topic that has been investigated over the past several years with increasing attention [1,2].
As disease-modifying drugs are crucially missing from the pipeline of treatments available for people with Alzheimer’s disease (AD) or related disorders, physicians, scientists, and public health experts are promoting the concept of early diagnosis.
Alzheimer’s disease (AD) transgenic mice have been used as a standard model for AD drug discovery and basic mechanistic studies. These mouse models overexpress amyloid β precursor protein (APP) or APP/presenilin (PS) with single or multiple familial AD (FAD) mutations, which lead to excess accumulation of amyloid β (Aβ), a well-known driver for AD pathogenesis.
The microtubule-associated protein tau is mainly expressed within neurons where it performs its physiological function of microtubule stability. However, extracellular tau is found in models of tau overexpression in which neuronal degeneration and cell death is prominent.
The field of Alzheimer research has reached an impasse after more than 100,000 clinical and scientific papers published in the last 40 years, because there is yet no hope, no effective treatment, and no knowledge of what causes this dementia.
For most people, older adulthood is associated with some decline in memory and in some aspects of cognitive function. These are age-related changes  that are widely expected, understood, and accepted by the general public.
Over the past few years there has been tremendous progress in diagnosis and therapeutic trials on Alzheimer’s disease (AD) and related dementias. Overall, the cost/benefit relationship is shifting with success.
Depression in Alzheimer’s disease (AD) has a substantial impact on disability, disease progression, and caregiver burden. Furthermore, depressive symptoms in normal aging, as well as in mild cognitive impairment (MCI), are associated with cognitive and functional decline.
Two hundred issues and nearly twenty years have positioned JAD at the center of printed and electronic peer-reviewed publications in Alzheimer's disease, as a venue that reflects the breadth of research in the field worldwide.