Alzheimer’s Dementia: An Overview

Abstract

Alzheimer’s disease (AD), the most common cause of dementia,
is a chronic illness characterized by cognitive symptoms, behavioural
and psychological symptoms and difficulty in performing activities
of daily living. Mild cognitive impairment (MCI) is regarded as a transitional
state between healthy cognitive ageing and dementia and around
12–15% of individuals with MCI progress to dementia annually. This
provides unique opportunity to initiate treatments targeted to delay or
prevent the onset of AD. Based on the age at onset, AD is divided into
two broad categories: early onset and late onset. Early onset AD follows
the classical mendelian pattern of inheritance, whereas the late onset
AD has a complex interplay of gene–environment interaction, with several
lifestyle-related risk factors strongly implicated in the pathogenesis
of this degenerative condition. The onset of AD pathology predates the
clinical symptoms by several years. The neurodegenerative processes
in AD is related to the accumulation of abnormally folded Aβ and tau
proteins in amyloid plaques and neuronal tangles. Diagnosis of AD is by
presence of cluster of clinical features and aided by biomarkers such as
CSF Aβ42 and PET amyloid imaging, CSF tau and tau imaging, 18fluorodeoxyglucose uptake on PET and atrophy on structural magnetic resonance imaging increase the diagnostic certainty. In the absence of
curative treatments, the management of AD involves pharmacological
treatment to delay the onset or progression of AD and supportive care by
family members. Targeting these lifestyle-related factors in young adulthood
and middle age may be protective against AD. High educational
achievement in early life, involvement in cognitively stimulating activity,
physical activity and social engagement including rich social network
have been associated with reduced risk of late-life dementia and AD.