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Related Concept Videos

Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
Dementia01:30

Dementia

Dementia is a collective term for cognitive disorders primarily affecting memory, thinking, and reasoning. It is not a specific disease but a syndrome, with Alzheimer's disease being the most common cause, accounting for approximately 60-80% of cases. Other types include vascular dementia, Lewy body dementia, and frontotemporal dementia. Dementia affects millions worldwide, particularly older adults, though it is not a normal part of aging.
The progression of dementia is generally gradual.
Alzheimer's Disease: Overview01:26

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 l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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...
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...

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Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
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Published on: June 3, 2020

Frontotemporal dementia: An updated overview.

E Mohandas1, V Rajmohan

  • 1Department of Psychiatry, Elite Mission Hospital, Koorkkencherry, Thrissur, Kerala, India.

Indian Journal of Psychiatry
|March 19, 2011
PubMed
Summary
This summary is machine-generated.

Frontotemporal dementia (FTD) is a progressive neurodegenerative disorder affecting individuals aged 45-65. Unlike Alzheimer's disease, FTD has a strong genetic basis, with no approved treatments currently available.

Keywords:
Frontotemporal dementiafrontotemporal lobar degenerationneurodegenerative disordersprogressive nonfluent aphasia

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Symmetric Bihemispheric Postmortem Brain Cutting to Study Healthy and Pathological Brain Conditions in Humans
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Last Updated: Jun 3, 2026

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Symmetric Bihemispheric Postmortem Brain Cutting to Study Healthy and Pathological Brain Conditions in Humans
08:29

Symmetric Bihemispheric Postmortem Brain Cutting to Study Healthy and Pathological Brain Conditions in Humans

Published on: December 18, 2016

Area of Science:

  • Neurology
  • Neuroscience
  • Genetics

Background:

  • Frontotemporal dementia (FTD), also known as frontotemporal lobar degeneration (FTLD), is a progressive neurodegenerative syndrome.
  • It typically affects individuals between 45 and 65 years old and is the third most common degenerative dementia.
  • FTD is characterized by atrophy of the prefrontal and anterior temporal cortices.

Purpose of the Study:

  • To summarize the key characteristics of Frontotemporal Dementia (FTD).
  • To highlight the genetic underpinnings and pathological features of FTD.
  • To outline the clinical presentation and current management approaches for FTD.

Main Methods:

  • Review of existing literature on Frontotemporal Dementia (FTD).
  • Analysis of epidemiological data, genetic linkage studies, and pathological classifications.
  • Summary of clinical symptoms and treatment strategies.

Main Results:

  • FTD affects 5-15% of dementia patients, with equal frequency in both sexes, typically onset between 45-65 years.
  • A strong genetic basis is observed in 40-50% of cases, with PGRN and MAPT genes on chromosome 17q21 being prevalent.
  • Behavioral changes are the most common initial symptom (62%), while speech and language issues dominate in related disorders.

Conclusions:

  • FTD is a genetically complex disorder with diverse pathologies and significant genetic contributions.
  • Current management relies on non-pharmacological interventions and caregiver support, as no approved drugs exist.
  • Further clinical trials are essential to identify effective therapeutic agents for FTD.