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Alzheimer’s disease and other forms of dementia

24 February 20246 January 2024 by Redazione My Special Doctor

DEMENCY is an organically based disturbance of previously acquired intellectual functions: memory (short- and long-term), critical and judgment skills, language, and spatio-temporal orientation.

Today, nearly 50 million people worldwide have some form of dementia, and this figure is set to rise to 75 million by 2030 and to 132 million by 2050, largely related to the aging of the population.

Dementia causes not only disability and dependence for people with the disorder, but it can also have a profoundly negative effect on family members e on all those who care for the affected person and who are at high risk of developing depression and anxiety disorders.

MAIN FORMS OF DEMENTIA

The Alzheimer’s disease
(AD) is the most common form of dementia. È 1906 the first description of the disease, by Alois Alzheimer: it concerned a 51-year-old woman, who presented simultaneously with cognitive deficits, psychiatric disorders and brain lesions ..

The disease affects 6 % of people over the age of 65 and 30 % of People over 80 years of age. It has a progressive course and the affected person survives for a maximum of 8-10 years. It is characterized by cerebral atrophy with significant reduction of the number of neuronal cells and synapses. In the brains of affected people, it is possible to detect the so-called senile plaques within which it is possible to detect, among other things, a toxic substance, the beta amyloid.

The disease begins with cognitive impairment e behavioral and the first symptom is usually impairment of recent memory. Next, other functions such as theattention, the concentration, l’abstraction, the skills of criticism and judgment, temporal-spatial orientation. In the more advanced stages, the following appear neurological deficits, such as difficulty in speaking particularly in naming objects (aphasia), difficulty in swallowing , (dysphagia) and in the final stages loss of autonomy.

Other diseases that cause progressive cognitive impairment include.

– The Lewy body dementia
is the second leading cause of dementia with between 10 and 20 percent of all dementia cases. The diagnostic criteria for LBD include a progressive dementia, visual hallucinations, parkinsonism and orthostatic hypotension..

– The hallucinations
are mostly visual, described as vivid, colorful and well-structured and, for this reason, also referred to as cinematic hallucinations. From a histological point of view, the pathology is characterized by the presence in the brain of Lewy bodies, intra-cytoplasmic inclusions consisting of alpha-synuclein

– The Fronto-temporal dementia
appears earlier than Alzheimer’s disease and can affect very young subjects even in their 30s with an average The prevalence in the population European population around the age of 60 years. It is characterized by progressive degeneration of certain brain districts such as the frontal and temporal lobes With cognitive decline and behavioral disturbances.

– The Vascular dementia: Cognitive impairment is related to impairment of brain structures by vascular pathologies, such as cerebral strokes, ischemic or hemorrhagic, or from lesions multiple lacunar related to pathologies of the small cerebral vessels. In many cases one can witness a “stepwise trend“, with sudden worsening related to new cerebrovascular events.

In elderly individuals, the vascular dementia can coexist with the typical signs of Alzheimer’s disease. This is the so-called mixed dementia that reflects the features of both AD and vascular dementia.

Given the initial difficulty of making a certainty diagnosis of Alzheimer‘s Disease: paricularly, efforts are being made to develop blood investigations aimed at revealing in the blood the presence of toxic substances such as beta-amyloid linked to Alzheimer’s disease. Although the accuracy is in recent studies close to 90%, the following are not to be ruled out false positives and false negatives. Can be used of the brain scans, but these in addition to being expensive have so far yielded contradictory results.

The main purpose of these investigations is primarily to arrive at an early diagnosis Of the disease. In fact, Alzheimer’s disease begins years before patients present with symptoms of memory loss.

The fundamental key to treating dementia is to diagnose the disease early before there is permanent loss of brain cells: Starting treatments in the disease stage could be completely futile

Although there is currently no treatment to modify the course of Alzheimer’s disease, identifying subjects at an early stage of the disease could also be useful in clinical trials because one could people are suitable for clinical trials and assess whether amyloid levels are amenable to change.

Lifestyles and prevention of Alzheimer’s disease (Lancet Commission on dementia prevention, intervention and care
. December 2017).

Occurrence of hearing loss in middle age – responsible for 9% of the risk
Low level of secondary education – 8%
Cigarette smoking – 5%
Presence of inadequately treated mood depression – 4%
Physical inactivity – 3%
Social isolation – 2%
Arterial hypertension – 2%
Obesity – 1%
Type 2 diabetes mellitus – 1%
These risk factors, which are described as potentially modifiable, affect up to 35 percent. Another 65% of dementia risk is in the potentially unmodifiable state

Good oral hygiene could help prevent Alzheimer’s disease

21 February 20246 January 2024 by Renato Torlaschi

According to surprising research published in the journal Science Advances, there is a significant link between the bacterium Porphyromonas gingivalis-the leading cause of periodontal disease-and Alzheimer’s disease.

In fact, a group of scientists from the University of Louisville, Kentucky, detected the presence of P. gingivalis in the brains of deceased people who had suffered from Alzheimer’s disease. The researchers also detected the bacterium’s Dna in spinal fluid and some toxic enzymes that are produced by the microorganism, gingipains, in the brain, where they measured higher levels of tau protein and ubiquitin, both linked to Alzheimer’s disease.

Interestingly, the brains of 50 cadavers used as controls, of elderly people who did not have Alzheimer‘s disease, had low levels of gingipain instead. This is an important result, because it is true that previous studies had already found an association between P. gingivalis and Alzheimer’s disease, but it was unclear whether poor oral care was only a side effect of dementia: it now appears that the opposite is true and that oral pathology may promote the development of Alzheimer’s disease.

For confirmation, the team conducted an experiment on laboratory mice for the purpose of testing whether P. gingivalis could enter the brain following oral infection and found that within six weeks this very passage occurred; they also observed dying nerve cells and high levels of beta-amyloid protein, a hallmark of Alzheimer’s disease.

The study does not prove that the bacterium causes Alzheimer’s, but that it is a likely contributing factor in the development of the disease.

“We know that diseases such as Alzheimer’s are complex and have multiple causes, but strong genetic evidence indicates that factors other than bacterial infections are central to the development of Alzheimer’s; therefore, these new findings need to be evaluated in the context of existing knowledge,” commented David Reynolds, scientific director of Alzheimer’s Research UK.

U.S. researchers even managed to find a way to kill P. gingivalis in the brains of mice; they used a compound targeting gingipain enzymes to successfully eliminate them, reduce neurodegeneration and beta-amyloid protein formation.

Alzheimer’s, a protein in the blood detects nerve cell degeneration

17 February 20246 January 2024 by Renato Torlaschi

A new study, recently published in JAMA Neurology, indicates that a simple blood test can reveal whether nerve cells in the brain are deteriorating at an abnormal rate. Researchers analyzed the presence of a protein, the so-called Neurofilament light Chain (NfL), in blood in patients with Alzheimer’s disease, finding a particularly high concentration of the protein.

Blood samples were collected over several years, and on several occasions, from 1,182 patients with varying degrees of cognitive impairment and 401 healthy subjects who made up the control group.

When nerve cells in the brain are damaged or die, the NfL protein enters the cerebrospinal fluid and then the blood: there were already suspicions about this, but long-term studies were lacking.

“We found that, in patients who develop Alzheimer’s disease, the concentration of NfL increases over time and that elevated levels correlate with the extent of accumulated brain damage,” said study coordinator Niklas Mattsson.

As is well known, Alzheimer’s is a complex disease that develops gradually and is difficult to analyze in its early, asymptomatic stages; the disease involves deterioration of cognitive and physical functions along with atrophy and death of brain cells. At present, there is no treatment that can reduce the loss of nerve cells in the brain, and available drugs are able to mitigate cognitive impairment but not slow the course of the disease. Measurements of NfL concentration in blood could be used to assess the effectiveness of a drug in influencing nerve cell loss and determine its optimal dosage.

Mattsson believes the method may soon translate into a standard clinical procedure: “at Sahlgrenska University Hospital in Gothenburg, we are doing the preparatory work to make this method available as a clinical procedure in the near future. Through a simple blood test, doctors will be able to measure nerve cell damage, produced by Alzheimer’s disease or other brain disorders.”.

Mattsson N, Cullen NC, Andreasson U, Zetterberg H, Blennow K. Association Between Longitudinal Plasma Neurofilament Light and Neurodegeneration in Patients With Alzheimer Disease. JAMA Neurol. 2019 Apr 22.

Correlation between cold sores and Alzheimer’s disease

18 February 20246 January 2024 by pcarrieri

The herpes simplex virus 1 often alters the face, putting those who are unfortunately affected in an uncomfortable condition. There is a tendency to hide one’s mouth, especially if one is in public places. There is no definitive cure to eradicate the virus from the body, so subsequent to infection you will be subject throughout your life to developing cold sores more or less frequently.

Educate You was among the very first in the country to report the results of an epidemiological study conducted in Taiwan by Dr. Ruth Itzhaki on a possible correlation between the disease of
Alzheimer’s disease
and the herpes simplex 1 virus, the very one responsible for the very annoying bubbles on the lips.

Confirmation now comes from a study conducted on experimental animals by Italian researchers, with Dr. Giovanna De Chiara of the National Research Council in Rome as the first name.

A model of recurrent herpes simplex virus 1 infections in mice that were subjected to repeated cycles of viral reactivation was used in this study. In the course of the study, a spread of the herpes simplex virus 1 also in different brain areas that resulted in the appearance in the brains of animals of some typical features of Alzheimer’s disease, including, most importantly, the protein-beta amyloid constantly present in the brains of people with Alzheimer’s disease. According to the authors, in mice infected with herpes simplex virus 1 The progressive accumulation of typical molecular changes in certain brain areas, including the cortex and hippocampus, correlates with the appearance and increase of cognitive deficits which become irreversible after seven cycles of virus reactivation. The authors conclude that repeated herpes simplex 1 infections could be considered as a risk factor for Alzheimer’s disease.

Source

De Chiara G et al. Recurrent herpes simplex virus-1 infection induces hallmarks of neurodegeneration and cognitive deficits in mice. PLoS Pathog. 2019 Mar 14;15(3):e1007617. doi: 10.1371/journal.ppat.1007617. eCollection 2019 Mar.

Alzheimer’s disease: beware of those drugs

15 February 20246 January 2024 by rosanna.feroldi

Despite intense research, the causes of Alzheimer ‘s disease continue to be essentially unknown. It has long been believed that mainly two protein factors, ß-amyloid plaques and Tau protein, are involved in its onset. But not all neurologists are convinced of this, and, in any case, it remains to be understood what determines the formation of these toxic substances for brain cells and what is their exact action.

Undoubtedly, the genetic predisposition individual plays an important role in determining the extent and speed of the cognitive decline, but study after study is becoming increasingly clear about the negative contribution of various environmental factors that can interfere with brain cell function and integrity, either directly or indirectly: from substances taken in with food to pollution, from sources of oxidative stress to drugs.

Precisely with regard to the latter, a new call for attention comes from a study conducted by researchers at the University of Nottingham (UK) who investigated the impact on intellectual performance and its age-associated deterioration of anticholinergic active ingredients-a class of drugs comprising molecules used to treat countless clinical conditions and whose use is widespread among the elderly.

They are anticholinergics, e.g., amitriptyline and paroxetine (two commonly used antidepressants), some antipsychotics (quetiapine, olanzapine, chlorpromazine), first-generation antihistamines such as promethazine (used against allergies and sleep disorders), furosemide (a diuretic indicated in cases of hypertension heart failure, and other diseases associated with water retention), amantadine (for the control of Parkinson’s disease), colchicine (prescribed for acute gout attacks), and baclofen (a centrally acting muscle relaxant).

Analyzing the medical records of some 58,800 patients diagnosed with dementia and 255,600 subjects without a diagnosis of dementia (all over the age of 55 and included in British family physician registries), the researchers found a correlation between taking anticholinergic drugs such as those mentioned above and increased risk of developing Alzheimer’s disease.

Specifically, people over 55 who had been chronically using these drugs for more than three years, at the higher dosages or in the “more active” versions, had a 50 percent higher risk of dementia over the next 10 years than those who had never taken them.

Responsible for the largest increase in the risk of Alzheimer’s disease were antipsychotics (+70%), antimuscarinics used against urinary incontinence (+65%), and anti-parkinsonian drugs (+52%), while antidepressants and antiepileptics seem to have a smaller, but still not negligible impact (+30% and +40%, respectively), especially in light of the fact that no effective therapies are currently available against Alzheimer’s disease.

How then to behave? Of course, if an anticholinergic drug is absolutely necessary to treat a significant health problem it must be used. But this need needs to be evaluated with caution, opting for safer alternative therapies whenever possible and, above all, avoiding administering these drugs chronically, over several years, if the benefit obtained is modest and not such as to justify the potential risks to brain health.

Source Coupland CAC et al. Anticholinergic Drug Exposure and the Risk of Dementia: A Nested Case-Control Study. JAMA Intern Med 2019; doi:10.1001/jamainternmed.2019.0677 (https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2736353?widget=personalizedcontent&previousarticle=2736349)

Alzheimer’s: a new blood test will allow diagnosis many years in advance

15 February 20246 January 2024 by Renato Torlaschi

Among the many critical issues related to Alzheimer’s disease, one concerns the difficulty of diagnosing it in its early stages. Although research has not yet identified a viable therapeutic approach, diagnostically the situation may soon change with the development of a blood test that scientists say can Diagnose up to 94 percent of Alzheimer’s cases 20 years earlier That the symptoms of the disease occur. The researchers in question are from Washington University in St Louis and described the test in the journal Neurology.

The disease is characterized by the increase ofbeta-amyloid plaques in the brain, associated with the accumulation of tau protein tangles, and the test proposed by the U.S. researchers relies precisely on the measurement of beta-amyloid in the blood, which would correlate with that in the brain .

The idea is not new and is a refinement of a technique already presented two years ago; it uses mass spectrometry to measure beta-amyloid-or, more precisely, the ratio between two forms of the protein, called A-β 42 and A-β 40 – and associates its blood concentration with two fundamental risk factors for developing Alzheimer’s: advanced age and the presence of a genetic variant called APOE4.

In this way, the accuracy of the test outperforms that of previous blood tests.

The team recruited 158 adults over the age of 50; all but 10 were described as cognitively normal. Each participant underwent at least one blood test and one PET scan with amyloid tracers , which is the current gold standard, and each test was labeled as amyloid positive or amyloid negative depending on the results produced.

Among experts, there is a growing consensus that in order to manage or treat Alzheimer’s, it is important to intercept it as early as possible, before symptoms begin to appear and the brain is not too damaged.

More than for a cure, which is not currently available, the test could further research. Today, to conduct clinical trials, we check people with scans, which is time-consuming and expensive, whereas with a blood test we could easily examine a large number of subjects, which would help us find treatments more quickly, with a huge potential impact.

Source: Schindler SE, Bollinger JG, et al. High-precision plasma β-amyloid 42/40 predicts current and future brain amyloidosis. Neurology. 2019 Aug 1.

Alzheimer’s disease: how to help those who help

14 February 20246 January 2024 by Redazione My Special Doctor

Caring for a loved one with health problems always has an ambivalent nature. On the one hand it makes you feel good because you have the awareness of helping in a time of need and offering support practical and psychological. On the other hand, however, it can “exhaust” physical energy and “inner resources,” especially when dealing with pathologies severe, associated with severe physical and/or mental suffering and of long duration. For its nature, Alzheimer’s disease demands a commitment from caregivers. particularly intense in the face of very little gratification, as the decline cognitive it entails is progressive and non-reversible, gradually subtracting also the ability to communicate. In order to be able to ensure valid support and prolonged, it is important that caregivers take care, in addition to the sick person, even of himself. Some advice .

Are you familiar with Alzheimer’s disease?

11 February 20246 January 2024 by Redazione My Special Doctor

It is becoming increasingly common, especially because of of the aging population, and much feared, because its effects on intellectual function are burdensome, and the available therapies do not still able to counter them effectively. For these reasons, of Alzheimer’s disease is much talked about, although, in reality, little is known about it. What this associated form of dementia really consists of. to aging? There are behaviors or substances that can help prevent it? How can it be recognized? And what should be expected from the treatments current? Try to test your knowledge with this quiz. , remembering that maintaining a healthy lifestyle and the active mind from a young age is the best insurance for aging in health.