How Frontotemporal Dementia Differs From Alzheimer’s

Frontotemporal Dementia Differs From Alzheimer’s

Although both frontotemporal dementia (FTD) and Alzheimer’s can result in dementia, the affected brain regions and, as a result, the symptoms differ significantly between the two. Knowing the differences between frontotemporal dementia and Alzheimer’s might assist in lowering the incidence of misdiagnosis, which may promote early treatment, better health outcomes, and improved life quality.

Understanding the distinction between Alzheimer’s and Frontotemporal Dementia

Dementia is an umbrella word used to represent a range of symptoms linked to a decline in memory, thinking, reasoning, or other cognitive skills rather than a specific disease. Frontotemporal dementia and Alzheimer’s are two of the several causes of dementia.

The Brain Regions They Affect

The fundamental distinction between frontotemporal dementia and Alzheimer’s is the brain regions they impact. Frontotemporal dementia, as its name suggests, predominantly affects the frontal and temporal lobes of the brain. The frontal and temporal lobes are typically related to personality, language, and behavior and are crucial for some cognitive processes. The frontal lobe is essential for performing higher-level executive functions, including judgment, reasoning, emotional regulation, and problem-solving. On the other hand, the temporal lobe plays a role in processing auditory data and encoding memories.

Contrarily, Alzheimer’s typically affects multiple brain regions with the disease progression. In the early stages, the disease affects the entorhinal cortex and hippocampus, which are critical for memory and learning. Later in the disease’s progression, it may deteriorate the cerebral cortex, which includes the frontal, parietal, temporal, and occipital lobes and is involved in memory, personality, behavior, language, speech, sensorimotor planning, spatial recognition, and visual perception and processing, among other things.

The Age of Onset

The timing of onset is another chief distinction between Alzheimer’s and frontotemporal dementia. Alzheimer’s affects adults aged 65 and over. The most significant risk indicator for acquiring Alzheimer’s is advancing age, but it is not a normal part of healthy aging. Contrarily, most patients with FTD are diagnosed between 40 and 60 years.

The Difference in Symptoms

Frontotemporal dementia and Alzheimer’s differ significantly; however, it can be difficult to distinguish between the two in clinical settings. Although early symptoms of FTD and Alzheimer’s can resemble one another in later stages, early stages are critical for getting an early, correct diagnosis since early stages symptoms are frequently quite different.

There are several differences between the symptoms of both disorders.

  • Memory loss is more prevalent in early Alzheimer’s than in early Frontotemporal dementia. However, advanced FTD frequently induces memory loss in addition to its more typical impact on language and behavior.
  • Behavioral changes are frequently the initial indications of bvFTD, the most prevalent type of FTD. Changes in behavior are frequent as Alzheimer’s advances, but they tend to appear later in the disease.
  • The occurrence of spatial orientation problems, such as becoming lost in familiar surroundings, is higher in Alzheimer’s than in FTD.
  • Although individuals with Alzheimer’s may struggle to find the proper word or remember names, they may experience less difficulty making sense when speaking, following others’ speech, or reading than those with FTD.
  • When Alzheimer’s disease worsens, delusions and hallucinations become more frequent; however, they are less common in FTD.

Memory loss is a common early indication of Alzheimer’s, whereas personality changes, behavioral problems, and linguistic difficulties are typical early signs of frontotemporal dementia. Also, it is crucial to remember that there are two main categories of FTD, each having a unique set of symptoms. Primary progressive aphasia (PPA) is related to a decline in speaking, language, writing, and comprehension, whereas behavioral variant frontotemporal dementia (bvFTD) is associated with behavior and personality changes.

The best likelihood of a successful therapeutic outcome, especially for Alzheimer’s, is thought to come from early diagnosis and intervention. The key to decreasing the rate of misdiagnosis and improving patient outcomes can be early and regular neurocognitive testing, employing highly-sensitive neurocognitive evaluations.

References

  1. How Is Frontotemporal Dementia Different From Alzheimer’s?. Altoida. https://altoida.com/blog/frontotemporal-dementia-different-from-alzheimers/. Published online: 8th Dec, 2022. Accessed: 27th March, 2023.
  2. Frontotemporal Dementia. Alzheimer’s Association. https://www.alz.org/alzheimers-dementia/what-is-dementia/types-of-dementia/frontotemporal-dementia. Accessed: 27th March, 2023.
  3. The Difference Between Alzheimer’s Disease and Frontotemporal Dementia. Assisted Hands. https://www.assistinghands-il-wi.com/blog/alzheimers-disease-vs-frontotemporal-dementia/.  Accessed: 27th March, 2023.

Fructose May Contribute to Alzheimer’s: Study

Fructose May Contribute To Alzheimer’s

According to a recent study from the University of Colorado Anschutz Medical Campus, increased fructose intake may be a chief cause of Alzheimer’s.

An ancient human foraging drive, fueled by fructose synthesis in the brain, may provide insights into Alzheimer’s development and potential treatment. The study1, published in The American Journal of Clinical Nutrition, provides a fresh perspective on a fatal condition distinguished by aberrant protein accumulations in the brain that gradually degrade memory and cognition.

The study’s lead author Richard Johnson, MD, a professor at the University of Colorado School of Medicine specializing in renal disease and hypertension, made the case that the diet drives Alzheimer’s. According to Johnson and his team, AD is a detrimental adaptation of a survival route that evolved in animals and our ancient ancestors to help them survive in times of scarcity.

Fructose: A Trigger For The Foraging Survival Response

Early humans had a survival reflex that sent them foraging for food when threatened with the risk of starvation. Yet, foraging is only productive if metabolism is suppressed in different brain regions. Focus, quick judgment, impulsivity, risk-taking, and exploratory behavior are necessary for foraging. It improves by obstructing anything that gets in the way, such as recent memories and time awareness. A type of sugar called fructose aids in calming these areas so that acquiring food can be the main focus.

The researchers discovered that fructose metabolism—whether it was consumed or created by the body—set the entire foraging response in action. It was essential for both humans and animals to metabolize fructose and its byproduct, intracellular uric acid.

The hippocampus, thalamus, and cerebral cortex of the brain that are involved in self-control all experience decreased blood flow as a result of fructose, according to the study’s authors. In the meantime, blood flow across the visual cortex related to food reward increased. Everything triggered the foraging response.

Researchers believed that initially, the fructose-dependent decrease in brain metabolism in these areas was reversible and intended to be advantageous. Yet, recurring fructose metabolism-driven chronic and permanent decline in cerebral metabolism causes progressive brain atrophy and cell death, symptoms of Alzheimer’s.

“Survival Switch” Remained In The “On” Position

Johnson hypothesizes that in an era of relative abundance, the survival reflex, or “survival switch,” that enabled prehistoric people to survive times of scarcity, is currently stuck in the “on” position. This results in excessive consumption of foods high in fat, sugar, and salt, which increases the creation of fructose.

According to the study, fructose generated in the brain may eventually cause inflammation and Alzheimer’s disease. When administered fructose, animals exhibit memory loss, decreased maze navigation skills, and neuroinflammation.

Johnson further stated that laboratory rats fed fructose for an extended period in a study developed the tau and amyloid beta proteins implicated in Alzheimer’s in their brains and that high fructose levels are also present in the brains of Alzheimer’s patients.

Johnson hypothesizes that certain AD patients’ propensity to wander off may be a trace of the primate foraging reflex.

The researchers proposed that both dietary and pharmaceutical trials to minimize fructose consumption or inhibit fructose metabolism be conducted to assess if there is potential benefit in the prevention, management, or treatment of this condition.

References

  • Johnson, R.J., Tolan, D.R., Bredesen, D., Nagel, M., Sánchez-Lozada, L.G., Fini, M., Burtis, S., Lanaspa, M.A. and Perlmutter, D., 2023. Could Alzheimer’s Disease Be a Maladaptation of an Evolutionary Survival Pathway Mediated by Intracerebral Fructose and Uric acid Metabolism?. The American Journal of Clinical Nutrition. https://www.sciencedirect.com/science/article/abs/pii/S0002916523000047.
  • Kelly, D. Study Suggests Fructose Could Drive Alzheimer’s Disease. University of Colorado Anschutz Medical Campus. https://news.cuanschutz.edu/news-stories/study-suggests-fructose-could-drive-alzheimers-disease. Published online: 13th Feb, 2013, Accessed: 6th March, 2023.
  • Fructose could drive Alzheimer’s disease. Science Daily. https://www.sciencedaily.com/releases/2023/02/230213113345.htm. Published online: 13th Feb, 2013, Accessed: 6th March, 2023.
  • Group of Scientists Propose a New Driver of Alzheimer’s Disease: Fructose. Science Alert. https://www.sciencealert.com/group-of-scientists-propose-a-new-driver-of-alzheimers-disease-fructose. Published online: 20th Feb, 2023. Accessed: 6th March, 2023.
  • Sugary Foods May Be Driving Alzheimer’s, Study Suggests. Psychiatrist.com. https://www.psychiatrist.com/news/sugary-foods-may-be-driving-alzheimers-study-suggests/. Published online: 20th Feb, 2023. Accessed: 6th March, 2023.

Neurologists Report World’s Youngest Alzheimer’s Case

World’s Youngest Alzheimer’s Case

Neurologists at a memory clinic in China have diagnosed a 19-year-old man with Alzheimer’s, making him the youngest person in the world with the condition.

According to a recent case study published in the Journal of Alzheimer’s Disease, a 19-year-old male from China who has had memory problems since age 17 was diagnosed with dementia.

Around age 17, the teen started experiencing memory deterioration and had difficulty concentrating on his high school studies. The cognitive decline worsened, and a year later, he started suffering from short-term memory loss.

The patient’s brain imaging revealed memory-related hippocampal shrinkage, and his cerebrospinal fluid suggested usual indicators of this most prevalent type of dementia.

Alzheimer’s is typically considered a disorder of the elderly. However, early-onset instances, which include people under the age of 65, account for up to 10% of all diagnoses.

Pathological gene mutations can explain Alzheimer’s in nearly all patients under 30, classifying them as having familial Alzheimer’s disease (FAD). The younger a person is at the time of diagnosis, the more likely it is due to an inherited defective gene.

When researchers from the Capital Medical University in Beijing analyzed the genome, they found no evidence of any normal mutations that cause early onset of memory loss, nor any problematic genes.

Before this recent diagnosis in China, the youngest Alzheimer’s patient was 21 years old. They had the PSEN1 gene mutation, which causes aberrant proteins to accumulate in the brain, generating toxic plaque clumps, a typical hallmark of Alzheimer’s disease.

The Tests Performed

Doctors working on the case dug deep into the teen’s medical and family history and conducted a series of tests to learn more about his illness. They discovered that he had a normal childhood development and that none of his parents, grandparents, or other relatives had a history of dementia, cognitive impairment, or psychiatric disease.

Doctors ruled out other common causes of cognitive impairment in young people, such as infection, inflammation, intoxication, trauma, abnormal metabolism, and “congenital abnormalities” because the patient had no history of head injuries, psychiatric or psychological disorders, or diseases associated with memory loss.

The teen also undertook MRI and CT scans, blood and urine analysis, cerebrospinal fluid (CSF) analysis, a tau tracer to look for tau tangles, and several neuropsychological tests for memory, mental state, anxiety, dementia, and depression.

His MRI revealed atrophy in the hippocampus—the loss of nerve cells and the connections that enable them to communicate in the brain’s tissues—and his CSF showed abnormal tau buildup.

Also, he performed worse than average on the World Health Organization-University of California, Los Angeles Auditory Verbal Learning Test, indicating a significant memory impairment.

To identify DNA mutations linked to early-onset Alzheimer’s, doctors sequenced the teenager’s and his family members’ genes but found none.

Rare Diagnosis

Alzheimer’s can occur sporadically due to heredity, aging, the environment, or pathogenic gene mutations.

Younger people are more likely to have these gene changes, as was the case with the previous youngest Alzheimer’s patient. As a result, specialists were perplexed by the teen’s diagnosis and the lack of any mutations. They said his instance had changed their knowledge of the average age of the disease onset.

The researchers did not specify what kind of treatment or assistance their young patient will receive, but they stated that they intend to follow up with him in the long term to understand the disease.

References

  • Jia, J., Zhang, Y., Shi, Y., Yin, X., Wang, S., Li, Y., Zhao, T., Liu, W., Zhou, A. and Jia, L., 2022. A 19-Year-Old Adolescent with Probable Alzheimer’s Disease. Journal of Alzheimer’s Disease, (Preprint), pp.1-8.
  • Agüero, P., Sainz, M.J., Téllez, R., Lorda, I., Ávila, A., García-Ribas, G., Rodríguez, P.P. and Gómez-Tortosa, E., 2021. De novo PS1 mutation (Pro436Gln) in a very early-onset posterior variant of Alzheimer’s disease associated with spasticity: A case report. Journal of Alzheimer’s Disease, 83(3), pp.1011-1016.
  • Neurologists Diagnose The Youngest Case of Alzheimer’s Ever Reported. Science Alert. https://www.sciencealert.com/neurologists-diagnose-the-youngest-case-of-alzheimers-ever-reported. Published online: 16th Feb, 23. Accessed: 3rd March, 23.
  • 19-year-old becomes youngest ever diagnosed with Alzheimer’s disease. National Post. https://nationalpost.com/health/19-year-old-youngest-ever-with-alzheimers. Published online: 16th Feb, 23. Accessed: 3rd March, 23.
  • Teenager in China becomes youngest person diagnosed with Alzheimer’s disease. CTV News. https://www.ctvnews.ca/health/teenager-in-china-becomes-youngest-person-diagnosed-with-alzheimer-s-disease-1.6281387. Published online: 21st Feb, 23. Accessed: 3rd March, 23.
  • A 19-year-old is the youngest person to be diagnosed with Alzheimer’s disease – the cause is a mystery. The Conversation. https://theconversation.com/a-19-year-old-is-the-youngest-person-to-be-diagnosed-with-alzheimers-disease-the-cause-is-a-mystery-200001. Published online: 22nd Feb, 23. Accessed: 3rd March, 23.

Brain Stimulation May Help Improve Alzheimer’s Symptoms: Study

Brain Stimulation May Help Improve Alzheimer’s Symptoms

Researchers at Charité – Universitätsmedizin Berlin have discovered a brain network that, when stimulated, can improve Alzheimer’s symptoms.

Deep brain stimulation (DBS) is a surgical procedure used to treat specific neurological diseases such as Parkinson’s disease, essential tremor, epilepsy, and dystonia. More than 160,000 individuals receive this therapy annually.

Several psychiatric conditions, such as drug addiction, obsessive-compulsive disorder (OCD), and treatment-resistant depression, have been the subject of prior studies that looked at DBS as a potential treatment.

Deep brain stimulation, administered by a pacemaker-like device, can also be one of the potential treatments for alleviating Alzheimer’s symptoms. A group of researchers at Charité – Universitätsmedizin Berlin has found that altering a particular network in the brains of Alzheimer’s patients can lessen their symptoms. The study, published in the journal Nature Communications, has provided hope for additional investigation in this area.

What is Deep Brain Stimulation (DBS)?

DBS is a surgical process in which doctors implant electrodes in a specific brain region of a person. These electrodes connect to wires that lead to an electric generator (similar to a cardiac pacemaker) inserted under a person’s collarbone.

The electrodes produce electric pulses that disrupt any aberrant signals the brain may receive that result in disease symptoms like tremors or movement difficulties.

DBS and Alzheimer’s

In a previous Canadian study about the use of DBS to treat obesity, the researchers discovered that DBS produced flashbacks to childhood memories in some study participants. They then investigated if stimulating this specific spot in the fornix portion of the brain could help treat Alzheimer’s. This observation became the basis of the current study.

The fornix houses the brain’s white matter. Previous studies have also linked fornix neurodegeneration to Alzheimer’s and looked into using DBS to stimulate that part of the brain to treat dementia.

The current study added to the body of knowledge by examining data from electrodes placed in the same area of the fornix in 46 persons with moderate Alzheimer’s disease.

Following an analysis, scientists reported no improvement in most patients’ symptoms. However, several people “benefited considerably” from the treatment. These participants had a specific brain circuit stimulated and showed cognitive benefits after treatment.

According to Dr. Horn, one of the authors, this retrospective study aims to determine the variations between participants in which the treatment performed better than others.

DBS therapy obstacles

What has prevented DBS from treating Alzheimer’s while the doctors are already employing it to treat neurological disorders like Parkinson’s? Dr. Jean-Philippe Langevin, a neurosurgeon and director of the Restorative Neurosurgery and Deep Brain Stimulation Program for Pacific Neuroscience Institute at Providence Saint John’s Health Center in Santa Monica, CA, has pointed out two chief reasons for this.

First, surgery is a more invasive and risky process than other therapies. The second is that DBS comes with an implantable device that needs adjustments, and often medical professionals struggle to use the programming devices.

He further pointed out that manufacturers have recently improved the software and device programmers, making them more user-friendly and intuitive.

What will be the next phases in DBS research?

Although DBS technology is advancing, it might still be some time before Alzheimer’s patients can get this treatment.

Dr. Horn stated that The ADvance II trial is presently underway in various centers worldwide. According to his understanding, if successful, it would increase the likelihood that the technique will receive both an FDA approval and a CE mark. As a result, many individuals who meet the requirements for which researchers have found DBS to be beneficial may be able to receive therapy.

Nevertheless, Dr. Horn cautioned that DBS is not a cure for neurodegenerative illnesses such as Parkinson’s or Alzheimer’s. Unfortunately, the disease will worsen, and the treatment will be symptomatic, at best helping to alleviate some of the symptoms for a short period.

References

  • Wang, T.R., Moosa, S., Dallapiazza, R.F., Elias, W.J. and Lynch, W.J., 2018. Deep brain stimulation for the treatment of drug addiction. Neurosurgical focus, 45(2), p.E11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329833/.
  • Mar-Barrutia, L., Real, E., Segalás, C., Bertolín, S., Menchón, J.M. and Alonso, P., 2021. Deep brain stimulation for obsessive-compulsive disorder: A systematic review of worldwide experience after 20 years. World journal of psychiatry, 11(9), p.659. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8474989/.
  • Roet, M., Boonstra, J., Sahin, E., Mulders, A.E., Leentjens, A.F. and Jahanshahi, A., 2020. Deep brain stimulation for treatment-resistant depression: Towards a more personalized treatment approach. Journal of Clinical Medicine, 9(9), p.2729. https://pubmed.ncbi.nlm.nih.gov/32846987/.
  • Ríos, A.S., Oxenford, S., Neudorfer, C., Butenko, K., Li, N., Rajamani, N., Boutet, A., Elias, G.J., Germann, J., Loh, A. and Deeb, W., 2022. Optimal deep brain stimulation sites and networks for stimulation of the fornix in Alzheimer’s disease. Nature Communications, 13(1), p.7707. https://www.nature.com/articles/s41467-022-34510-3