Sure thing! Alzheimer's and the eyes may seem unrelated at first, but there's an interesting connection between the two. Recent research suggests that changes in the eyes, such as thinning of the retinal nerve fiber layer, may be linked to the development and progression of Alzheimer's disease. Some scientists believe that examining the eyes could potentially serve as a non-invasive way to detect early signs of Alzheimer's. It's a fascinating intersection of neuroscience and ophthalmology!

1. OCULAR MANIFESTATIONS IN
ALZHEIMER’S DISEASE
ANUJA DHAKAL
OPTOMETRIST

2. LAYOUT
• Introduction
• Pathophysiology
• Ocular structural changes
• Ocular functional visual changes

3. INTRODUCTION
• Alzheimer’s disease (AD) is the most common form of dementia affecting the
growing aging population today, with prevalence expected to rise over the next 35
years.
• Clinically, patients exhibit a progressive decline in cognition, memory, and social
functioning due to deposition of amyloid β (Aβ) protein and intracellular
hyperphosphorylated tau protein.
• AKA senile dementia of the Alzheimer’s type(SDAT).

4. • Presently, AD can only be diagnosed post-mortem on histo-pathological
examination. Diagnostic investigations are limited, and physicians rely on clinical
examination and exclusion of differential diagnoses that may cause cognitive
impairment, such as
Depression,
Parkinson’s disease (PD),
Hypothyroidism,
Drug interactions, and
Vitamin deficiencies .
• Clinically, a diagnosis is made based on history, examination, and where available,
accounts from relatives or carers.

6. PATHOPHYSIOLOGY
Two signature lesions :
1)Neuritic plaques/ B – amyloid plaques
Deposition of extracellular senile plaques, which is composed of amyloid
β (Aβ)
2)Neurofibrillary tangles (NFT’S), build up inside the nerve cell
Resulting from intracellular (intraneuronal) aggregates of
hyperphosphorylated tau protein detected in the brain.

7. NEUROBIOLOGICAL MECHANISMS
Mutations Environmental factors
Amyloid precursor protein
Amyloidogenic peptides
Oligomers
Amyloid plaques
Tau pathology
Neuronal death
Amyloidogeneic proteolysis
Aggregration
Aggregration
Synaptic
Neurotransmitters
Alterations

8. OCULAR ANATOMICAL CHANGES WITH
ALZHEIMER’S
1. TEARFILM: Change in chemical barrier composition of tears
2. CORNEA: Reduced corneal sensitivity
3. AQUEOUS HUMOUR :Presence of β-amyloid peptides&chemokines
4. PUPIL: Atypical response to cholinergic antagonists
Lower amplitude and latency to light reflex
Pupillary mydriasis.

9. 5. LENS: Deposition of β-amyloid
Predisposition to supranuclear cataract
6. RETINA : Decreased retinal blood flow
RNFL thinning
Ganglion cells degeneration & reduction in axons
B-amyloid deposition in retina
Deposition of : TAU, Aβ ,PTAU
Reduced in retinal thickness
Retrograde degeneration of cortical neurons
Inflammation.

10. 7) CHOROID : Reduction/ Attenuation of choroidal thickness
Choroidal vascular B-amyloid deposits.
8) OPTIC NERVE : Axonal degeneration
Loss of optic nerve thickness
Papillary paleness(increased pallor )
Increased Cup-Disc ratio
Affect in Magnocellular pathway
Optic disc atrophy in absence of Glaucoma.

11. VISUAL PATHWAY CHANGES
9. LATERAL GENICULATE NUCLEUS : Lipofuschin accumulation
Resistance to tangle formation
10. SUPRACHIASMATIC NUCLEUS : Degeneration
11. VISUAL CORTEX : Myelin reduced in outer laminae
Loss of pyramidal cells
12. B17 : Numerous cored senile plaques but few Tangles.

12. FUNCTIONAL VISUAL CHANGES
1. VISUAL ACUITY: Decreased in low luminance
2. VISUAL FIELD: Inferior hemi-field loss
3. STEREOPSIS: Reduced stereopsis, mean threshold >150” arc
4. COLOUR VISION: Poor colour discrimination
Deficiency in tritan axis (blue-violet)
Incomplete achromatopsia

13. 5. CONTRAST SENSITIVITY: Reduced contrast sensitivity in low luminance
Reduced reading speed in low contrast.
6. MOTION PERCEPTION: Higher threshold for motion detection in all spatial
frequencies
7. SACCADES: Abnormal hypometric saccades
Abnormal saccadic initiation
Delayed peak velocity
8. PURSUIT :Impaired with intrusion of saccades
Increased latency

14. 9. VISUAL MASKING: Significantly affected by backward masking
10. FIXATION: Affected
11. EYE-HEAD CO-ORDINATION: Impaired
12. ERG: Reduction of wave amplitude in pattern ERG
13. CORTICAL VEP: Normal P100 latency & delayed flash P2 latency

15. 14. VISUOSPATIAL: Deficits observed in 40-50%
15. VISUAL HALLUCINATIONS: 20% of people experience it
16. CIRCADIAN RHYTHM: Alterations in circadian rhythm
B-amyloid deposits around degenerative mRGCs

16. THANK YOU