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FRONTOTEMPORAL DEMENTIA

Last Updated on 18th December, 2023
7 minutes, 32 seconds

Description

FRONTOTEMPORAL DEMENTIA

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Picture Courtesy: www.alzheimercalgary.ca

Context: An international team of researchers, which includes specialists from Indiana University School of Medicine, has discovered a protein that is present in the brains of patients with frontotemporal dementia (FTD). This discovery reveals a new potential target for developing treatments for FTD.

Details

  • The research findings shed light on a significant discovery regarding frontotemporal dementia (FTD) and its association with a protein called TAF15. This protein has been identified to form amyloid filaments in nerve cells of the brain and spinal cord, contributing to neurodegenerative disorders.

Key Points

  • Nature of FTD: FTD, a type of dementia, results from neuronal injury in the brain's frontal and temporal lobes. It manifests with symptoms like unusual behaviours and emotional disturbances, often appearing in individuals aged 25 to 65.
  • Role of TAF15: The study reveals that TAF15 protein forms amyloid filaments in brain and spinal cord cells in cases of FTD, potentially leading to the onset of this type of dementia.
  • Research Methodology: The team, utilizing advanced cryo-electron microscopy (cryo-EM) at atomic resolution, examined protein aggregates from the brains of individuals with FTD and motor weakness. Their analysis identified the presence of TAF15 amyloid filaments in multiple brain regions, including nerve cells of the motor system.
  • Significance of Discovery: Neuropathologist highlights the importance of this breakthrough. Recognizing TAF15 as a potential target opens avenues for diagnostic and therapeutic strategies to address this lesser-known form of frontotemporal lobar degeneration linked with FTD.

Implications

  • Diagnostic Advancements: Understanding the role of TAF15 in FTD can aid in developing diagnostic tools for early detection of this form of dementia.
  • Therapeutic Prospects: Identification of TAF15 as a potential target could lead to the development of therapeutic interventions to mitigate or prevent the progression of FTD associated with this protein.
  • Research Direction: This discovery may pave the way for further investigations into TAF15-related mechanisms underlying FTD and related neurodegenerative disorders.

Frontotemporal dementia

  • Frontotemporal dementia (FTD) is a term that covers a range of brain disorders that affect the frontal and temporal lobes of the brain, which are responsible for personality, behaviour and language.
  • FTD is different from Alzheimer's disease, which mainly affects memory and cognition.
  • It usually starts at a younger age, between 40 and 65 years old, and can cause dramatic changes in how a person thinks, acts and communicates.
  • Some people with FTD may also develop movement problems, such as stiffness, tremors, muscle weakness or difficulty swallowing. These symptoms are similar to those seen in Parkinson's disease or amyotrophic lateral sclerosis (ALS).
  • In some cases, FTD may be linked to genetic mutations or inherited from a family member.

Diagnosis

  • The diagnosis of FTD can be challenging, as it can be mistaken for other conditions, such as depression, bipolar disorder or schizophrenia.
  • There is no specific test for FTD, but doctors may use brain scans, blood tests, neuropsychological tests and interviews to rule out other causes and identify the type of FTD.
  • The progression of FTD varies from person to person, but it usually worsens over time and leads to severe disability and dependence.

Cure

  • There is no cure for FTD, but there are treatments that can help manage the symptoms and improve the quality of life of people with FTD and their caregivers. These include medications, behavioural therapies, speech therapy, occupational therapy and physical therapy.
  • Support groups, counselling and education can also help people cope with the emotional and social challenges of living with FTD.

Human Brain

●The human brain can be divided into three main parts: the cerebrum, the cerebellum, and the brainstem. Each part has a different role and is made up of several subparts.

Cerebrum

The cerebrum is the largest and most visible part of the brain. It occupies the upper part of the skull and consists of two hemispheres (left and right) that are connected by a bundle of nerve fibres called the corpus callosum.

It is covered by a thin layer of grey matter called the cerebral cortex, which has many folds and grooves to increase its surface area.

●The cerebral cortex is responsible for higher cognitive functions such as reasoning, language, creativity, and problem-solving. It also processes sensory information from the eyes, ears, nose, skin, and other organs.

Cerebellum

●The cerebellum is located at the lower back of the brain, below the cerebrum. It is smaller than the cerebrum but has more neurons (nerve cells).

It is responsible for coordinating movement, balance, posture, and fine motor skills. It also plays a role in learning and memory.

Brainstem

The brainstem is located at the base of the brain, where it connects to the spinal cord. It consists of three parts: the midbrain, the pons, and the medulla oblongata.

●The brainstem is responsible for controlling vital functions such as breathing, heart rate, blood pressure, digestion, swallowing, coughing, sneezing, and vomiting. It also regulates sleep cycles and consciousness.

Conclusion

  • The research represents a significant step forward in unravelling the molecular mechanisms behind FTD, offering potential avenues for targeted treatments and an improved understanding of this complex neurological condition.

PRACTICE QUESTION

Q. What is the role of the TAF15 protein in Frontotemporal Dementia (FTD)?

A) It causes vascular abnormalities in the brain.

B) It forms amyloid filaments in nerve cells.

C) It regulates neurotransmitter release.

D) It induces inflammation in the brain.

Answer: B

Explanation: Research indicates that TAF15 protein plays a role in the development of amyloid filaments in individuals with FTD.

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