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Related Concept Videos

Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
Parkinson's Disease: Treatment01:24

Parkinson's Disease: Treatment

Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of its...
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Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
Parkinson's Disease: Overview01:15

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Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is to...

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Updated: May 25, 2026

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia
07:18

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Published on: November 9, 2018

Treatment options for tauopathies.

Tarik Karakaya1, Fabian Fußer, David Prvulovic

  • 1Department of Psychiatry, J.W. Goethe-University, Heinrich-Hoffmann-Str. 10, 60528, Frankfurt, Germany, tarik.karakaya@kgu.de.

Current Treatment Options in Neurology
|February 7, 2012
PubMed
Summary
This summary is machine-generated.

Currently, no approved treatments exist for tauopathies like progressive supranuclear palsy (PSP), frontotemporal dementia (FTD), and corticobasal degeneration (CBD). Research is exploring tau protein pathology as a promising therapeutic target.

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Area of Science:

  • Neuroscience
  • Neurology
  • Pharmacology

Background:

  • Tauopathies, including progressive supranuclear palsy (PSP), frontotemporal dementia (FTD), and corticobasal degeneration (CBD), are heterogeneous neuropsychiatric disorders often presenting as atypical Parkinson syndromes.
  • Currently, no pharmacologic treatments are approved for tauopathies, with existing strategies relying on limited evidence from small trials and case reports, often yielding contradictory results.

Purpose of the Study:

  • To review current treatment strategies for tauopathies.
  • To highlight the limitations of existing therapies and the need for novel approaches targeting the underlying disease mechanisms.

Main Methods:

  • Review of available literature on pharmacologic and non-pharmacologic interventions for tauopathies.
  • Analysis of off-label use of medications approved for Alzheimer's dementia and Parkinson's disease.
  • Discussion of symptomatic treatments for cognitive, behavioral, and motor symptoms.

Main Results:

  • Off-label use of acetylcholinesterase inhibitors and memantine for cognitive symptoms in tauopathies shows inconsistent outcomes.
  • Levodopa and dopamine agonists are used for motor symptoms, while selective serotonin reuptake inhibitors may help with behavioral issues.
  • Antipsychotics carry significant risks and should be used cautiously due to adverse effects and increased cerebrovascular event risk in tauopathies.

Conclusions:

  • Current treatment for tauopathies is largely symptomatic and individualized, with no therapies targeting the disease's root cause.
  • Physical, occupational, and speech therapies can improve functional abilities.
  • Emerging research focusing on tau protein pathology, such as aggregation and phosphorylation, shows promise for future therapeutic development.