Dementia of Alzheimer type :- Definitions :- Dementia is a clinical syndrome characteurd by global cognitive decline with memory and one ather area of cognition affected that interfere significantly with person's ability to perform the tasks of daily life. Dementia resulting from Alzeimer's visto disease or DAT is characterised by decline primarily in cortical aspects of cognition (i.e. memory, language, praxis) 4 Follows a a characteristic time course of gradual Onset and progression. Alyleimer's disease is a specific degener alve brain disease characterised by senile plaques, neuritic tangles, and progressive loss of neurons, the presumptive cause of Alzheimer's disease. Pathophysiology: Algheimer's disease is characterised by the loss of neurons and synapses in the
if the cerebral cortex and certain subcortical regions. This loss results in gross atrophy of affected regions, including degeneration in the temporal lobe and parietal lobe and. parts of frontal cortex and cingulated ggrus. haha • Gross pathophysiological changes: - cortical atrophy enlarged rentides - basal ganglia wasting. Microscopically: changes in the proteins of the nerve cells of the cerebral cortex. accumulation of neuro fibrillary tangles and neuritic plaques. - granulovascular degeneration. - loss of cholinergic nerve cells. (import ant in memory, function, cognition) The main pathological hallmarks of Alzheimer's disease : - extracellular deposition of ß-amyloid , (AB) plaques. - Intraneuronal neurofibrillary tangles, .
Newritic Plaques :- cleared by B-secretase a-secretase mutation of amyloid precursor protein on chromosome no. 21 s Increased production of amyloid precursor protein tein x-secretase has 2 genes 1 142, when these undergoes mutation, they lead to increased clearing of a Secretase. These increased clearing of App results | in increased production of ß-amyloid protein ! Produces amybid protein Accumulation B-amyloid of in. protein Directly neuro to xin Alzheimer's disease Neuro fibrillary tangles :- • Neurons have an internal Support Shucture partly made up of microtubules. A protein called tau helps stabilize microtubules. In AD, tau changes, causing microtubules to collapse, a tau proteins clump together to form neuro fibrillary tangles n o Further research, particularly in the genetic domain, led to identification of APP and Presenilin genes (APP, PSENI & PENZ) 4 mutations in these genes as cause of rare forms of early-onset familial AD.
. On other hand, Eu allele of apolipoprotein E gene CAPOE) has been recognised as a major risk factor for late onset AD. Clinical manifestations : Signs : · Memory loss • Difficulty to performing familiar tasks • Problems with language. • Disorientation to time and place · poor or decreased judgement • Problems with abstract thinking Mis placing things • changes in mood or behavior Changes in personality. · loss of inihabire. Symptoms • Confusion distrabance in short-term memory problems with attention and spatial personality change more d orlentation. language difficulties. un explained mood swings. Evaluation : Psychiatric assessments. Mental status examination psychological assessment . laboratory test. and neuro-
Brain maging - CT scan - MRI - PET - SPECT · CSF examination · Electroencephalo gram (EEG) • Electromyogram . Treatment 1. Caregiving: Since Alzheimer's has no cure and it gradually renders people incapable of tending for their own needs, caregiving essentially is the treatment and must be carefully managed over the course of the disease 2. Pharmacological intervention! (a) Acetylcholinesterase inhibitors - prevent the break down of acetylcholine. a chemical messenger important for learning and memory. eg: Donepezil Rivastigmine e Galantamine (b) N-methyl a- aspartate Receptor Antagonist (NMDA) eg: Methr Memantine the (6) Anti-depressants (d) Anxiolytics (1) Antipsychotics (f) Ants convulsants.
3. Psychosocial intervention :- • Behavioral approach • Emotional oriented approach - Remnisence therapy - validation therapy - supportive psychotherapy - sensory integration - Stimulated presence therapy cognition oriented approach Stimulation oriented approach